ライフサイエンスコーパス: Werner

1 Werner and Bloom syndromes are genetic RecQ helicase dis

2 Werner and Bloom syndromes are human diseases characteri

3 Werner protein (WRN) is a member of the recQ gene family

4 Werner syndrome (WRN) is an uncommon autosomal recessive

5 Werner syndrome (WRN) is an uncommon autosomal recessive

6 Werner Syndrome (WS) and Bloom Syndrome (BS) are disorde

7 Werner syndrome (WS) is a genetic premature aging disord

8 Werner syndrome (WS) is a human genetic disorder charact

9 Werner Syndrome (WS) is a human genetic disorder with ma

10 Werner syndrome (WS) is a human premature aging disorder

11 Werner syndrome (WS) is a human premature aging disorder

12 Werner Syndrome (WS) is a human progeroid disorder chara

13 Werner syndrome (WS) is a human progeroid syndrome chara

14 Werner syndrome (WS) is a premature aging disorder cause

15 Werner syndrome (WS) is a premature aging disorder where

16 Werner syndrome (WS) is a premature aging disorder, disp

17 Werner syndrome (WS) is a premature aging syndrome cause

18 Werner syndrome (WS) is a progeroid-like syndrome caused

19 Werner syndrome (WS) is a rare autosomal recessive disor

20 Werner syndrome (WS) is a rare disease caused by the lac

21 Werner syndrome (WS) is a rare human premature aging dis

22 Werner syndrome (WS) is a rare progeroid disorder charac

23 Werner syndrome (WS) is a recessive disorder characteriz

24 Werner syndrome (WS) is an accelerated ageing disorder w

25 Werner syndrome (WS) is an autosomal recessive disease c

26 Werner syndrome (WS) is an autosomal recessive disease c

27 Werner syndrome (WS) is an autosomal recessive disease t

28 Werner syndrome (WS) is an autosomal recessive genetic d

29 Werner syndrome (WS) is an inherited disease characteriz

30 Werner Syndrome (WS) is an inherited disease characteriz

31 Werner syndrome (WS) is an inherited disorder characteri

32 Werner syndrome (WS) is characterized by features of pre

33 Werner Syndrome (WS) is characterized by premature aging

34 Werner syndrome (WS) is characterized by premature onset

35 Werner syndrome (WS) is characterized by the early onset

36 Werner syndrome (WS) is marked by early onset of feature

37 Werner syndrome (WS) is the canonical adult human proger

38 Werner syndrome (WS) is the hallmark premature aging dis

39 Werner syndrome (WS), caused by loss of function of the

40 Werner syndrome (WS), caused by mutations of the WRN gen

41 Werner syndrome and Bloom syndrome result from defects i

42 Werner syndrome arises through mutations in the WRN gene

43 Werner syndrome is a disorder characterized by genomic i

44 Werner syndrome is a genetic condition of young adults c

45 Werner syndrome is a genetic disorder characterized by g

46 Werner syndrome is a hereditary disorder characterized b

47 Werner syndrome is a hereditary premature aging disorder

48 Werner syndrome is a hereditary premature aging disorder

49 Werner syndrome is a human disorder characterized by pre

50 Werner syndrome is a human premature aging disorder disp

51 Werner syndrome is a Mendelian disorder of man that prod

52 Werner syndrome is a premature aging and cancer-prone he

53 Werner Syndrome is a premature aging disorder characteri

54 Werner Syndrome is a premature aging disorder characteri

55 Werner syndrome is a rare autosomal recessive disease ch

56 Werner syndrome is a rare human disease characterized by

57 Werner syndrome is an autosomal recessive disorder assoc

58 Werner syndrome is an inherited disease displaying a pre

59 Werner syndrome is associated with mutations in the DNA

60 Werner syndrome is associated with premature aging and i

61 Werner syndrome is genetically linked to mutations in WR

62 Werner syndrome protein (WRN) is a RecQ-type DNA helicas

63 Werner syndrome protein (WRN) plays critical roles in DN

64 Werner syndrome, caused by mutations of the WRN gene, mi

65 Werner's syndrome (WS) and Bloom's syndrome (BS) are can

66 Werner's syndrome (WS) is a human disease with manifesta

67 Werner's syndrome (WS) is an autosomal recessive disorde

68 Werner's syndrome (WS) is an inherited disease character

69 Werner's syndrome is a progeroid syndrome caused by muta

70 The chromosome 8p11-12 Werner syndrome (WRN ) locus encodes a RecQ helicase pro

71 Although describable as a Werner Mn(V) complex, analysis by X-ray diffraction, mag

72 In addition to its DNA helicase activity, Werner syndrome protein (WRN) also possesses an exonucle

73 WRN protein involved in the premature aging Werner syndrome, do not exhibit the gene cluster instabi

74 ated incidence of cancer or premature aging: Werner syndrome, Bloom syndrome, and Rothmund-Thomson sy

75 Alfred Werner defined the basics of coordination chemistry, wor

76 Alfred Werner's complexes of formula [M(III)(NH(3))(6-n)X(n)]X(

77 As reported by Alfred Werner in 1911-1912, salts of the formally D3 symmetric

78 ition-metal complexes originates from Alfred Werner's realization that their three-dimensional shape

79 it was not until the late 1800s when Alfred Werner published his ground-breaking research on coordin

80 rma overlap syndrome 100 kDa autoantigen and Werner syndrome protein.

81 ence with the RecQ helicases Bloom (Blm) and Werner (Wrn).

82 icases, which includes the Bloom's (BLM) and Werner's (WRN) syndrome gene products, are apparently un

83 (G4 resolvase 1), Bloom helicase (BLM), and Werner helicase (WRN).

84 Here we show that purified Bloom and Werner helicases can unwind a DNA triple helix.

85 ecQ-like DNA helicases such as the Bloom and Werner syndrome genes, BLM and WRN, have been suggested

86 line mutations are responsible for Bloom and Werner syndromes, respectively.

87 are mutated, respectively, in the Bloom and Werner syndromes, whose manifestations include predispos

88 cQ helicases, which are mutated in Bloom and Werner's syndrome, respectively, and associated with chr

89 e (BS), Rothmund-Thomson syndrome (RTS), and Werner syndrome (WS).

90 family helicases encoded by the Bloom's and Werner's syndrome genes are likely to act in concert wit

91 BLM and WRN, the products of the Bloom's and Werner's syndrome genes, are members of the RecQ family

92 RecQ helicases such as the human Bloom's and Werner's syndrome proteins and that copies of the helica

93 ve implications for the basis of Bloom's and Werner's syndromes, which are caused by mutations in DNA

94 ed DNA-binding protein RPA, and the Srs2 and Werner/Bloom helicases, but not Ku and ligase 4.

95 Bloom syndrome and Werner syndrome are genome instability disorders, which

96 solve these structures in Bloom syndrome and Werner syndrome cells may contribute to genome instabili

97 e products of the human Bloom's syndrome and Werner's syndrome genes.

98 that includes the human Bloom's syndrome and Werner's syndrome proteins.

99 m, Cockayne's syndrome, Bloom's syndrome and Werner's syndrome, have been linked to defects in specif

100 and cancer susceptibility syndrome known as Werner syndrome (WS).

101 es associated with premature ageing, such as Werner's syndrome and Hutchinson-Gilford progeria syndro

102 th the human RecQ helicase diseases, such as Werner, Bloom, and Rothmund-Thomson syndromes, are also

103 mology to the WRN exonuclease domain, atWEX (Werner-like Exonuclease).

104 ilford Progeria Syndrome (HGPS) and Atypical Werner Syndrome.

105 in Hutchinson-Gilford progeria and atypical Werner syndromes.

106 ions and were categorised as having atypical Werner's syndrome on the basis of molecular criteria.

107 sequenced LMNA in individuals with atypical Werner's syndrome (wild-type WRN).

108 Individuals with atypical Werner's syndrome with mutations in LMNA had a more seve

109 In four (15%) of 26 patients with atypical Werner's syndrome, we noted heterozygosity for novel mis

110 in humans, which include RECQ1, Bloom (BLM), Werner (WRN), RECQ4, and RECQ5.

111 licase family that includes the human Bloom, Werner, and Rothmund-Thompson syndrome proteins.

112 hat include the determinants of human Bloom, Werner, and Rothmund-Thomson syndromes, the shortened li

113 Five paralogues (RecQ1, Bloom, Werner, RecQ4, and RecQ5) are found in human cells, with

114 ify molecules that modulate DNA unwinding by Werner syndrome helicase (WRN), mutated in the premature

115 utations in the chromosome 8p WRN gene cause Werner syndrome (WRN), a human autosomal recessive disea

116 Mutations in the WRN gene cause Werner syndrome, a genetic disorder characterized by pre

117 ion mutations in the WRN helicase gene cause Werner syndrome- a progeroid syndrome with an elevated r

118 Mutations of wrn cause Werner syndrome (WS), an autosomal recessive premature a

119 WRN protein loss causes Werner syndrome (WS), which is characterized by prematur

120 of the RecQ DNA helicase WRN protein causes Werner syndrome, in which patients exhibit features of p

121 tational inactivation of the gene WRN causes Werner syndrome, an autosomal recessive disease characte

122 remature ageing phenotypes that characterize Werner syndrome.

123 t), telomere dysfunction elicits a classical Werner-like premature aging syndrome typified by prematu

124 or metal ions, forming normally coordinative Werner-type bonds by utilizing the N donor atoms of the

125 Acrolein decreased Werner's syndrome protein (WRN), a member of the RecQ he

126 n (WRN) leads to the premature aging disease Werner syndrome (WS).

127 The cancer-prone and premature aging disease Werner syndrome is due to loss of WRN gene function.

128 nuclease, causes the premature aging disease Werner syndrome.

129 The premature aging and cancer-prone disease Werner syndrome is caused by loss of function of the Rec

130 The premature aging and cancer-prone disease Werner syndrome stems from loss of WRN protein function.

131 he premature aging and cancer-prone diseases Werner and Bloom syndromes are caused by loss of functio

132 The human premature aging disorder Werner syndrome (WS) is associated with a large number o

133 s a hallmark of the premature aging disorder Werner syndrome (WS).

134 RN), mutated in the premature aging disorder Werner syndrome.

135 mature aging and genome instability disorder Werner syndrome, encodes a protein with DNA helicase and

136 n causes the cancer-prone progeroid disorder Werner syndrome (WS).

137 The segmental, progeroid disorder Werner syndrome results from loss of the Werner syndrome

138 manifest as a rare premature aging disorder, Werner syndrome.

139 e premature aging and cancer-prone disorder, Werner syndrome.

140 associated with a rare, recessive disorder, Werner syndrome (WS), distinguished by premature aging a

141 e responsible for the cancer-prone disorders Werner syndrome and Bloom syndrome.

142 damage that has previously been observed for Werner's syndrome cells.

143 a- and UV-irradiation, suggesting a role for Werner protein in stress-induced gene expression.

144 from normal (young and old) donors and from Werner syndrome (WS) patients.

145 Cells from Werner syndrome patients are characterized by slow growt

146 We recently discovered that cells from Werner syndrome patients displayed a deficiency in p53-m

147 s with mutations in the WRN gene suffer from Werner syndrome, a disease with early onset of many char

148 We argue that Heinz Werner's classical research on the physiognomic properti

149 me result from defects in the RecQ helicases Werner (WRN) and Bloom (BLM), respectively, and display

150 Here, Werner protein (WRN) was identified as a novel target fo

151 Herlyn-Werner-Wunderlich syndrome is a rare congenital urogenit

152 maging modalities in diagnosis of the Herlyn-Werner-Wunderlich syndrome with a review of literature.

153 Hutchinson-Gilford progeria syndrome (HGPS), Werner syndrome, Bloom syndrome, Cockayne syndrome, tric

154 This review discusses how Werner coordination chemistry plays a role in three dise

155 Human Werner Syndrome is characterized by early onset of aging

156 es, such as human Bloom's syndrome and human Werner's syndrome helicases.

157 These adducts inhibited the human Werner (WRN) syndrome helicase activity in a strand-spec

158 licases, including yeast Sgs1p and the human Werner and Bloom syndrome proteins, participate in telom

159 The human Werner and Bloom syndromes (WS and BS) are caused by def

160 Moreover, it is a homologue of the human Werner syndrome gene product WRN, a protein associated w

161 rectly stimulates transcription of the human Werner syndrome gene, WRN, which encodes a conserved Rec

162 The human Werner syndrome protein, WRN, is a member of the RecQ he

163 eening data of cancer cell lines we identify Werner syndrome helicase (WRN) as a novel specific vulne

164 factor contributing to accelerated aging in Werner and Bloom syndromes, but not XFE progeroid syndro

165 VX-745 against p38alpha MAPK is confirmed in Werner syndrome dermal fibroblasts at 1.0 microM concent

166 and BLM gene products that are defective in Werner and Bloom syndromes, disorders which share many p

167 Werner protein (WRN), which is defective in Werner syndrome ( WS) patients, belongs to the RecQ fami

168 ns of the WRN and BLM helicases defective in Werner syndrome and Bloom syndrome, respectively, have b

169 the replication and recombination defects in Werner syndrome cells may reflect abnormal processing of

170 4 complex), and WRN the protein deficient in Werner syndrome.

171 ligase IIIalpha, and the protein deleted in Werner syndrome, WRN, are up-regulated.

172 The gene mutated in Werner syndrome encodes both a 3' --> 5' DNA helicase an

173 The WRN helicase/exonuclease is mutated in Werner syndrome of genomic instability and premature agi

174 ease nuclear localization of WRN (mutated in Werner syndrome), which is required for processing DSB e

175 3'-->5' exonuclease and helicase mutated in Werner syndrome, a disorder characterized by aberrant te

176 iation of WRN, the factor that is mutated in Werner syndrome.

177 encodes a RecQ helicase, which is mutated in Werner syndrome.

178 Terc mutants but similar to that observed in Werner syndrome and Bloom syndrome, such as bone loss, w

179 structures that resemble defects observed in Werner syndrome, a premature ageing disorder.

180 ontribute to the various defects observed in Werner's and Bloom's syndromes.

181 mic instability and cancer predisposition in Werner syndrome cells.

182 in APLF that we now show is also present in Werner syndrome protein (WRN) and in Modulator of retrov

183 genomic instability, which are prominent in Werner and Bloom syndromes.

184 Mutations in the WRN gene result in Werner syndrome, an autosomal recessive disease in which

185 e accelerated replicative senescence seen in Werner syndrome (WS) fibroblasts is due to accelerated t

186 , which is compromised by the loss of WRN in Werner syndrome.

187 number of human genetic disorders, including Werner Syndrome, Bloom Syndrome and Rothmund-Thomson Syn

188 lta processivity was enhanced by full length Werner Syndrome protein (WRN) and by WRN fragments conta

189 er predisposition and/or shortened lifespan (Werner, Bloom, and Rothmund-Thomson syndromes).

190 iated gas clouds that are exposed to a Lyman-Werner intensity roughly three times the intensity of th

191 ture formation, rather than a critical Lyman-Werner flux, is the main driver of the formation of mass

192 namical heating(13,14), amplifying the Lyman-Werner suppression that originates from a group of young

193 Mgs1, the budding yeast homolog of mammalian Werner helicase-interacting protein 1 (WRNIP1/WHIP), con

194 function of the RecQ helicase family member Werner syndrome protein (WRN).

195 ses result in Bloom Syndrome (BLM mutation), Werner Syndrome (WRN mutation), Rothmund-Thomson Syndrom

196 d DNA double-strand breaks in the absence of Werner syndrome (WRN) protein, and that it interacts phy

197 c disruption of the WRN gene is the cause of Werner disease.

198 are warranted to mitigate this component of Werner and Bloom syndromes.

199 national registry for molecular diagnosis of Werner's syndrome, 26 (20%) had wildtype WRN coding regi

200 etabolic dysfunction is a primary feature of Werner syndrome (WS), a human premature aging disease ca

201 f rapidly dividing cells is not a feature of Werner syndrome.

202 Thus, manifestations of Werner syndrome may reflect an impaired ability of slowl

203 roposed to contribute to the pathogenesis of Werner syndrome (WS), a premature-aging disorder.

204 nction may contribute to the pathogenesis of Werner syndrome and Bloom syndrome.

205 te telomere attrition in the pathogenesis of Werner syndrome.

206 The clinical phenotype of Werner Syndrome (WRN) includes features reminiscent of a

207 Cellular phenotypes of Werner syndrome and Bloom syndrome, including genomic in

208 he varied and complex cellular phenotypes of Werner syndrome are precipitated by exhaustion of telome

209 To map regions of Werner syndrome helicase (WRN) that interact with RPA, y

210 ularly nonepithelial malignancies typical of Werner syndrome.

211 osine (dA) or N(2) of deoxyguanosine (dG) on Werner (WRN) syndrome helicase activity.

212 the recent gene-driven phase of research on Werner syndrome, a heritable adult progeroid syndrome wi

213 Upon DNA unwinding by Bloom (BLM) or Werner (WRN) helicase, RPA directs the DNA2 nuclease to

214 cs of cells from individuals with Bloom's or Werner's syndrome.

215 In particular, Werner syndrome helicase and related genes are different

216 One in particular, Werner syndrome, provides evidence to support the hypoth

217 WRN, which is absent in the human progeroid Werner syndrome, is thought to counteract this genomic i

218 ions on the catalytic activities of purified Werner (WRN) and Bloom (BLM) DNA helicases.

219 RN and RECQ4 genes are defective in Bloom's, Werner's and Rothmund-Thomson syndromes, respectively.

220 een linked to three human diseases: Bloom's, Werner's and Rothmund-Thomson's syndromes.

221 BLM, WRN, and RECQL4 are mutated in Bloom's, Werner, and Rothmund Thomson syndromes, respectively.

222 er predisposition diseases, causing Bloom's, Werner, and Rothmund-Thomson syndromes.

223 2F3.1); and (4) the WRN subgroup (H. sapiens Werner and C. elegans F18C5.2).

224 ive human genetic disorders (Bloom syndrome, Werner syndrome and Rothmund-Thomson syndrome, respectiv

225 the genomic instability progeroid syndrome, Werner syndrome.

226 instability/cancer predisposition syndromes Werner syndrome and Bloom syndrome.

227 Our findings indicate that Werner's syndrome is molecularly heterogeneous, and a su

228 The Werner and Bloom syndromes are caused by loss-of-functio

229 The Werner protein (WRN) belongs to the RecQ family of DNA h

230 The Werner protein (WRN), which is defective in Werner syndr

231 The Werner syndrome (WS) is a prototypic adult Mendelian pro

232 The Werner syndrome (WS) is an autosomal recessive segmental

233 The Werner syndrome and the Nijmegen breakage syndrome are r

234 The Werner syndrome helicase (WRN) participates in DNA repli

235 The Werner syndrome protein (WRN) is a caretaker of the huma

236 The Werner syndrome protein (WRN) is a RecQ family helicase

237 The Werner syndrome protein (WRN) is the only known member o

238 The Werner syndrome protein (WRN) suppresses the loss of tel

239 The Werner syndrome protein, WRN, is a member of the RecQ fa

240 the RNA-dependent RNA polymerase QDE-1, the Werner and Bloom RecQ DNA helicase homologue QDE-3 and d

241 In addition, the Werner syndrome protein (WRN) possesses an exonuclease a

242 ction between the AAA ATPase p97/VCP and the Werner protein (WRNp), a member of the RecQ helicase fam

243 stability of the multicopy transgene and the Werner Syndrome gene.

244 human DNA polymerase eta (hpol eta) and the Werner syndrome protein (WRN).

245 DNA Polymerase delta (Pol delta) and the Werner syndrome protein, WRN, are involved in maintainin

246 the human Bloom's syndrome gene BLM and the Werner's syndrome gene WRN.

247 in the premature aging disease known as the Werner syndrome is designated WRN and is a member of the

248 DNA2 acts with RecQ helicases such as the Werner syndrome protein (WRN) and the heterotrimeric euk

249 Mutations at the Werner helicase locus (WRN) are responsible for the Wern

250 hich hpol kappa activity is modulated by the Werner syndrome protein (WRN), a RecQ helicase known to

251 one of our most promising dependencies, the Werner syndrome ATP-dependent helicase, as a synthetic l

252 We now report that Ku enables the Werner exonuclease to digest through regions of DNA cont

253 caused by mutations in the gene encoding the Werner (WRN) DNA helicase.

254 f, and contrapodal to, the gene encoding the Werner syndrome helicase, Wrn, at human chromosome band

255 helicase locus (WRN) are responsible for the Werner syndrome (WS).

256 f BLM, or another G4-unwinding helicase, the Werner syndrome-associated helicase WRN, resulted in inc

257 A defect in the Werner syndrome protein (WRN) leads to the premature agi

258 Cells deficient in the Werner syndrome protein (WRN) or BRCA1 are hypersensitiv

259 rived B cells that contained variants in the Werner syndrome, RecQ helicase-like gene (WRN, encoding

260 at three RecQ members (WRN, deficient in the Werner syndrome; BLM, deficient in the Bloom syndrome; a

261 Q DNA helicase family that also includes the Werner syndrome protein, WRN.

262 useful in association studies involving the Werner syndrome (WRN) gene.

263 te here that the stimulating activity is the Werner syndrome protein (WRN).

264 The prototypic example of the former is the Werner syndrome, a condition caused by mutations of the

265 e helicase and exonuclease activities of the Werner protein (WRN) suggest that it functions in DNA tr

266 The yeast homologue of the Werner protein (WRN), Sgs1, is required for recombinatio

267 WRN) and a deficiency in the function of the Werner protein (WRN).

268 FFA-1 is the orthologue of the Werner syndrome gene product (WRN), a member of the RecQ

269 thods and present a transcription map of the Werner syndrome gene region.

270 der Werner syndrome results from loss of the Werner syndrome protein (WRN).

271 ogy with the FEN-1 interaction domain of the Werner syndrome protein, a RecQ helicase family member h

272 Mutants for sgs1, the yeast homolog of the Werner's syndrome gene, accumulate ERCs more rapidly, le

273 Research on the Werner syndrome and a surprising number of other progero

274 Evidence suggests that the Werner syndrome protein (WRN) contributes to the mainten

275 Our previous studies indicated that the Werner syndrome protein (WRN) interacts with Ku, a heter

276 In this study, we provide evidence that the Werner syndrome protein (WRN) physically interacts with

277 We show here that the Werner syndrome protein (WRN), a member of the RecQ fami

278 se activity and ability to interact with the Werner protein (WRN) and telomere-binding protein (TRF2)

279 during S phase when it colocalizes with the Werner syndrome gene product, WRN, in the nucleolus.

280 Ku70/80 interacts with the Werner syndrome protein (WRN) and stimulates WRN exonucl

281 asmids with noncompatible ends introduced to Werner syndrome cells underwent extensive deletions at n

282 the human WRN gene, whose mutation leads to Werner syndrome resembling premature aging.

283 ny-forming assay in which a SV40-transformed Werner fibroblast cell line is 6-18-fold more sensitive

284 in the human RECQ3 gene result in truncated Werner protein (WRN) and manifest as a rare premature ag

285 (NO3 )6 (M=Al, Ga) can be synthesized using Werner's century-old cluster as a substitutable framewor

286 one of the clinical findings associated with Werner syndrome.

287 s, including the WRN protein associated with Werner's syndrome, might also adopt ring structures.

288 FEN1, abolished the interaction of FEN1 with Werner syndrome protein (WRN), an interaction that is cr

289 fibroblasts cultured from an individual with Werner's syndrome.

290 ence of cultured cells from individuals with Werner syndrome and the lack of a disease phenotype in W

291 g and old individuals and from patients with Werner syndrome (WS), a segmental progeroid condition wi

292 n profiles occur in cells from patients with Werner syndrome and from normally aged individuals.

293 teristic of cells derived from patients with Werner syndrome.

294 Persons with Werner syndrome displays premature aging of the skin, va

295 we identified the DNA repair protein WRNIP1 (Werner helicase-interacting protein 1), along with nucle

296 Mechanistically, Xenopus Werner syndrome protein (xWRN) is required for the unwin

297 cases, the major one of which is the Xenopus Werner syndrome protein (xWRN), a member of the RecQ hel

298 acts on ssDNA unwound mainly by the Xenopus Werner syndrome protein (xWRN), xEXO1 acts directly on d

299 s (ss-tails) by stimulating both the Xenopus Werner syndrome protein (xWRN)-mediated unwinding of DNA

300 We also found that the Xenopus Werner syndrome protein, a member of the RecQ helicase f