ライフサイエンスコーパス: Bloom

1 Bloom bacterioplankton also transcribed more copies of g

2 Bloom bacterioplankton transcribed more copies of genes

3 Bloom cell lines show increased sister chromatid exchang

4 Bloom decline is also accompanied by increased activity

5 Bloom dilution may provide a mechanistic explanation for

6 Bloom protein (BLM) is a 3'-5' helicase, mutated in Bloo

7 Bloom protein (BLM) is a 3'-5' helicase, mutated in Bloo

8 Bloom syndrome (BS) is a genetic disorder associated wit

9 Bloom syndrome (BS) is a genetic disorder that predispos

10 Bloom syndrome (BS) is a hereditary disorder characteriz

11 Bloom syndrome (BS) is a rare autosomal recessive disord

12 Bloom syndrome (BS) is a rare cancer-predisposing disord

13 Bloom syndrome (BS) is a rare genetic disorder character

14 Bloom syndrome (BS) is an autosomal recessive disorder c

15 Bloom syndrome (BS) is an autosomal recessive disorder c

16 Bloom syndrome (BS) is characterized by genomic instabil

17 Bloom syndrome (BS) is more frequent in the Ashkenazic J

18 Bloom syndrome (BS), an autosomal recessive disorder, is

19 Bloom syndrome and Werner syndrome are genome instabilit

20 Bloom syndrome confers strong predisposition to malignan

21 Bloom syndrome is a disorder associated with genomic ins

22 Bloom syndrome is a disorder of profound and early cance

23 Bloom syndrome is a familial genetic disorder associated

24 Bloom syndrome is a rare autosomal disorder characterize

25 Bloom syndrome is a rare disorder associated with cancer

26 Bloom syndrome is a rare, autosomal recessive inherited

27 Bloom Syndrome is an autosomal recessive cancer-prone di

28 Bloom syndrome is an autosomal recessive disorder associ

29 Bloom syndrome is an autosomal recessive disorder caused

30 Bloom syndrome patients have a strong predisposition to

31 Bloom Syndrome, a rare human disorder characterized by g

32 Bloom syndrome, characterized by a predisposition to can

33 Bloom's helicase (BLM) is thought to prevent crossing-ov

34 Bloom's syndrome (BS) and Fanconi anemia (FA) are autoso

35 Bloom's syndrome (BS) is a disorder associated with chro

36 Bloom's syndrome (BS) is a genetic disorder associated w

37 Bloom's syndrome (BS) is a genetic disorder characterize

38 Bloom's syndrome (BS) is a human genetic disorder associ

39 Bloom's syndrome (BS) is a rare autosomal recessive diso

40 Bloom's syndrome (BS) is a rare autosomal recessive diso

41 Bloom's syndrome (BS) is a rare autosomal recessive gene

42 Bloom's syndrome (BS) is a rare human genetic disorder c

43 Bloom's syndrome (BS) is a rare recessive disorder cause

44 Bloom's syndrome (BS) is an autosomal recessive disorder

45 Bloom's syndrome (BS) is an autosomal recessive disorder

46 Bloom's syndrome (BS) is an autosomal recessive disorder

47 Bloom's syndrome (BS) is an autosomal recessive disorder

48 Bloom's syndrome (BS), a disorder associated with genomi

49 Bloom's syndrome helicase (BLM) is a member of the RecQ

50 Bloom's syndrome is a genetic disorder characterized by

51 Bloom's syndrome is a hereditary cancer-predisposition d

52 Bloom's syndrome is a human autosomal genetic disorder c

53 Bloom's syndrome is a rare autosomal recessive disorder

54 Bloom's syndrome is a rare autosomal recessive genetic d

55 Bloom's syndrome is a recessive human genetic disorder a

56 Bloom's syndrome is caused by mutations in the BLM gene.

57 h AU rich elements) (RHAU) (G4 resolvase 1), Bloom helicase (BLM), and Werner helicase (WRN).

58 sclerosis complex, neurofibromatosis type 1, Bloom syndrome, epidermolytic hyperkeratosis, X-linked i

59 A complex of human topoisomerase 3alpha, Bloom helicase, and RecQ-mediated genome instability pro

60 Similarly, a Bloom syndrome helicase (BLM) domain fragment, BLM(642-1

61 s based on a probabilistic data structure, a Bloom filter, that allows us to efficiently store assemb

62 oth groups were similar with respect to age, Bloom-Richardson score, Estrogen Receptor status, adjuva

63 e 2 groups were similar with respect to age, Bloom-Richardson score, estrogen receptor status, use of

64 the effects of an Ecosystem Disruptive Algal Bloom (EDAB) on the microbial community separated from s

65 on to the false-positive rates common to all Bloom filter-based approaches.

66 However, topoisomerase III alpha and Bloom helicase can dissolve DNA conjoined with a double

67 otein complex of topoisomerase III alpha and Bloom helicase.

68 Fanconi anemia and Bloom syndrome are genomic instability syndromes caused

69 ntifying FANCM as the anchor for both FA and Bloom's complexes at the site of the DNA interstrand cro

70 Fanconi Anemia (FA) and Bloom Syndrome share overlapping phenotypes including sp

71 Fanconi Anemia (FA) and Bloom's Syndrome (BS) are genetic disorders characterize

72 Fanconi anemia (FA) and Bloom's syndrome (BS) are rare hereditary chromosomal in

73 similarities between Fanconi Anemia (FA) and Bloom's Syndrome, identifying FANCM as the anchor for bo

74 by enzyme immunoassay, tumor histology, and Bloom-Richardson grade.

75 fix arrays for creating smaller indexes, and Bloom filters for speeding up sequence search.

76 syndromes such as xeroderma pigmentosum and Bloom syndrome as well as Werner's syndrome, in which pa

77 Two RecQ helicases, RECQL5 and Bloom syndrome mutated (BLM) suppress HR through nonredu

78 the various defects observed in Werner's and Bloom's syndromes.

79 nce paradigm modeled after Egan, Santos, and Bloom (2007).

80 Werner syndrome and Bloom syndrome result from defects in the RecQ helicases

81 Cellular phenotypes of Werner syndrome and Bloom syndrome, including genomic instability and premat

82 M helicases defective in Werner syndrome and Bloom syndrome, respectively, have been extensively inve

83 ilar to that observed in Werner syndrome and Bloom syndrome, such as bone loss, was observed.

84 e cancer-prone disorders Werner syndrome and Bloom syndrome.

85 e to the pathogenesis of Werner syndrome and Bloom syndrome.

86 predisposition syndromes Werner syndrome and Bloom syndrome.

87 , microstructure, water content, texture and Bloom of sucrose free white chocolate was investigated.

88 rt a specific interaction between TopBP1 and Bloom syndrome helicase (BLM) that is phosphorylation an

89 pendent RNA polymerase QDE-1, the Werner and Bloom RecQ DNA helicase homologue QDE-3 and dicers.

90 cluding yeast Sgs1p and the human Werner and Bloom syndrome proteins, participate in telomere biology

91 The human Werner and Bloom syndromes (WS and BS) are caused by deficiencies i

92 e aging and cancer-prone diseases Werner and Bloom syndromes are caused by loss of function of WRN an

93 The Werner and Bloom syndromes are caused by loss-of-function mutations

94 Werner and Bloom syndromes are genetic RecQ helicase disorders char

95 Werner and Bloom syndromes are human diseases characterized by prem

96 tributing to accelerated aging in Werner and Bloom syndromes, but not XFE progeroid syndrome.

97 ne products that are defective in Werner and Bloom syndromes, disorders which share many phenotypic a

98 stability, which are prominent in Werner and Bloom syndromes.

99 an important protein interaction of WRN and Bloom syndrome (BLM) helicases is with the structure-spe

100 ytic activities of purified Werner (WRN) and Bloom (BLM) DNA helicases.

101 fects in the RecQ helicases Werner (WRN) and Bloom (BLM), respectively, and display premature aging p

102 Werner's syndrome (WS) and Bloom's syndrome (BS) are cancer predisposition disorder

103 of mouse embryonic stem (ES) cells that are Bloom's syndrome protein (Blm) deficient.

104 d lower atmosphere during the North Atlantic Bloom Experiment in the spring 2008 from samples collect

105 and zooplankton tracking the North Atlantic Bloom in May 2008.

106 BLM (Bloom's syndrome protein), a RecQ DNA helicase, and topo

107 ster chromatid while the RecQ helicase, BLM (Bloom syndrome mutated) suppresses crossing over to prev

108 -efficient manner by using a pattern-blocked Bloom filter to remove infrequent k-mers from considerat

109 egard to clinical parameters, including BRE (Bloom, Richardson, Elston) grade, nodal status, estrogen

110 Mutations in BLM cause Bloom's syndrome, a disorder associated with cancer pred

111 cular basis of missense mutations that cause Bloom's syndrome, a human RecQ-associated disease.

112 f BLM, a helicase of the RecQ family, causes Bloom syndrome, a genetic disorder with a strong predisp

113 d in cancer predisposition diseases, causing Bloom's, Werner, and Rothmund-Thomson syndromes.

114 is, and reduced formation of foci containing Bloom syndrome helicase (BLM) after hydroxyurea-induced

115 A variant of method can resort to a counting Bloom filter for even larger savings in memory at the ex

116 at have been linked to three human diseases: Bloom's, Werner's and Rothmund-Thomson's syndromes.

117 d BLM mutation causes the heritable disorder Bloom's syndrome.

118 s rise to the cancer predisposition disorder Bloom's syndrome.

119 ersons with the autosomal recessive disorder Bloom syndrome are predisposed to cancers of many types

120 A human genetic disorder, Bloom's syndrome, is associated with a defect in one mem

121 als with the cancer predisposition disorder, Bloom's syndrome (BS).

122 of the human cancer predisposition disorder, Bloom's syndrome.

123 autosomal recessive human genetic disorders (Bloom syndrome, Werner syndrome and Rothmund-Thomson syn

124 icated in the genetic instability disorders, Bloom syndrome (BS), Rothmund-Thomson syndrome (RTS), an

125 r mutagen-sensitive) encoding the Drosophila Bloom's syndrome helicase homolog (DmBLM) and the Ku70 g

126 Genetic analysis of the Drosophila Bloom's syndrome helicase homolog (mus309/DmBLM) indicat

127 The gene for Bloom syndrome (BLM) has been mapped to human chromosome

128 olytic hyperkeratosis, and a mouse model for Bloom syndrome are reviewed in this article.

129 which germline mutations are responsible for Bloom and Werner syndromes, respectively.

130 in ES cells lacking the gene responsible for Bloom syndrome, an inherited DNA repair defect that resu

131 Cells from Bloom's syndrome patients display genome instability due

132 when both MUS81 and SLX4 were depleted from Bloom's syndrome cells, suggesting that GEN1 can compens

133 ild-type cells but not in cells derived from Bloom syndrome patients with inactivating BLM mutations.

134 enesis system demonstrate that extracts from Bloom's syndrome (BS) cells are unable to use microhomol

135 on is attenuated in primary fibroblasts from Bloom syndrome patients.

136 on of MUS81 and GEN1, or SLX4 and GEN1, from Bloom's syndrome cells results in severe chromosome abno

137 Here we deplete these nucleases from Bloom's syndrome cells to analyse human cells compromise

138 activate a process that required functional Bloom's syndrome-associated (BLM) helicase, Mus81 nuclea

139 The mutated gene, Bloom protein (BLM), encodes a DNA helicase that functio

140 cy for either of the genomic stability genes Bloom's syndrome helicase or DNA ligase 4, and the effec

141 as does interference with the RecQ helicases Bloom (Blm) and Werner (Wrn).

142 vity but did not affect other DNA helicases [Bloom syndrome (BLM), Fanconi anemia group J (FANCJ), RE

143 uplex DNA unwinding helicases, such as human Bloom's syndrome and human Werner's syndrome helicases.

144 coli RecQ protein and the products of human Bloom's syndrome and Werner's syndrome genes.

145 Sgs1, the orthologue of human Bloom's syndrome helicase BLM, is a yeast DNA helicase f

146 zymes that include the determinants of human Bloom, Werner, and Rothmund-Thomson syndromes, the short

147 which encodes the yeast homolog of the human Bloom helicase, or in mismatch repair (MMR) genes confer

148 ophila Dmblm locus is a homolog of the human Bloom syndrome gene, which encodes a helicase of the REC

149 Like the human Bloom syndrome helicase (BLM), Sgs1 functions during bot

150 , including Escherichia coli RecQ, the human Bloom syndrome protein (BLM), and Saccharomyces cerevisi

151 homology to RecQ helicases such as the human Bloom's and Werner's syndrome proteins and that copies o

152 hich also includes the products of the human Bloom's syndrome and Werner's syndrome genes.

153 ily of DNA helicases that includes the human Bloom's syndrome and Werner's syndrome proteins.

154 es a DNA helicase with homology to the human Bloom's syndrome gene BLM and the Werner's syndrome gene

155 DNA helicase family that includes the human Bloom, Werner, and Rothmund-Thompson syndrome proteins.

156 In Bloom's syndrome, this phenotype manifests as an elevate

157 Analysis of BLM in Bloom's syndrome fibroblasts or by depletion of BLM from

158 BLM, the helicase defective in Bloom syndrome, is part of a multiprotein complex that p

159 BLM, the gene defective in Bloom's syndrome, encodes a 159-kDa protein possessing D

160 BLM, the gene that is defective in Bloom's syndrome, encodes a protein homologous to RecQ s

161 he BLM, WRN and RECQ4 genes are defective in Bloom's, Werner's and Rothmund-Thomson syndromes, respec

162 gesting a basis for the immune deficiency in Bloom's syndrome.

163 overs include the RecQ helicase deficient in Bloom syndrome cells (BLM), which is part of a complex t

164 The recent cloning of the genes involved in Bloom syndrome (BLM) and Werner syndrome (WRN) show that

165 n Daxx and BML, the RecQ helicase missing in Bloom syndrome, as new ND10-associated proteins.

166 o human RecQ helicases, which are mutated in Bloom and Werner's syndrome, respectively, and associate

167 own WRN or BLM (the RecQ helicase mutated in Bloom syndrome) expression in primary human fibroblasts.

168 coated by BLM (the RecQ helicase mutated in Bloom syndrome) in early mitosis.

169 BLM, the helicase mutated in Bloom syndrome, associates with topoisomerase 3alpha, RM

170 BLM, the gene mutated in Bloom syndrome, has been cloned previously, and the BLM

171 e that BLM, the RecQ DNA helicase mutated in Bloom syndrome, is preferentially modified by SUMO-2/3 b

172 rotein (BLM) is a 3'-5' helicase, mutated in Bloom syndrome, which plays an important role in respons

173 rotein (BLM) is a 3'-5' helicase, mutated in Bloom syndrome.

174 The BLM gene mutated in Bloom's syndrome encodes a DNA helicase involved in the

175 The gene mutated in Bloom's syndrome, BLM, encodes a DNA helicase (BLM) of t

176 The gene mutated in Bloom's syndrome, BLM, encodes a member of the RecQ fami

177 The product of the gene mutated in Bloom's syndrome, BLM, is a 3'-5' DNA helicase belonging

178 BLM, a RecQ family DNA helicase mutated in Bloom's Syndrome, participates in homologous recombinati

179 BLM, the protein mutated in Bloom's syndrome, possesses a helicase activity that can

180 homologs BLM, WRN, and RECQL4 are mutated in Bloom's, Werner, and Rothmund Thomson syndromes, respect

181 Mutations in Bloom helicase (BLM) lead to Bloom Syndrome (BS).

182 The attenuated apoptotic phenotype in Bloom syndrome cells was rescued not only by ectopic exp

183 ed the high rate of mitotic recombination in Bloom's syndrome protein (Blm)-deficient ES cells to gen

184 he human BLM gene, whose mutation results in Bloom syndrome, and the human WRN gene, whose mutation l

185 ontaneous sister chromatid exchange (SCE) in Bloom syndrome (BS) cells, but not in their BLM-correcte

186 r SLX4 reduces the high frequency of SCEs in Bloom's syndrome cells, indicating that MUS81 and SLX4 p

187 that failure to resolve these structures in Bloom syndrome and Werner syndrome cells may contribute

188 d cancer predisposition syndromes, including Bloom syndrome, caused by mutations affecting the BLM pr

189 trial, we genotyped 3,258 SNPs in 10 Jewish Bloom syndrome cases and 31 non-Bloom syndrome Jewish pe

190 icase family, Dmblm (Drosophila melanogaster Bloom), which encodes a putative 1487-amino-acid protein

191 %Su and 75%St+25%Su samples showed a minimum Bloom formation, probably due to its dense microstructur

192 zygous for a targeted mutation in the murine Bloom's syndrome gene (Blm) are developmentally delayed

193 in 10 Jewish Bloom syndrome cases and 31 non-Bloom syndrome Jewish persons as a comparison group.

194 It uses a pair of cache oblivious Bloom filters, one holding a uniform sample of [Formula:

195 Mus81 is essential in the absence of Bloom's syndrome Rqh1 helicase and is required for produ

196 findings have implications for the basis of Bloom's and Werner's syndromes, which are caused by muta

197 sister chromatid exchange characteristic of Bloom's syndrome.

198 atid exchange (SCE)--the hallmark feature of Bloom syndrome cells.

199 A defining feature of Bloom's syndrome is an elevated frequency of sister chro

200 a predisposition to cancer are hallmarks of Bloom syndrome, an autosomal recessive disease arising f

201 microstructure and the highest percentage of Bloom was observed.

202 mented the genomic instability phenotypes of Bloom syndrome cells as assessed by sister-chromatid exc

203 explains many of the cellular phenotypes of Bloom's syndrome.

204 he first time the possible predisposition of Bloom syndrome patients with impaired PKM2 activity to c

205 hich is needed for subsequent recruitment of Bloom syndrome protein (BLM) and exonuclease 1 (Exo1) to

206 e believe that a more nuanced model based on Bloom's taxonomy is better suited to EHL and to future r

207 We report kinetic studies on Bloom (BLM) helicase and human telomeric GQ interactions

208 HR (breast cancer associated gene, Brca2, or Bloom's syndrome, Blm) for sensitivity to trichostatin A

209 he help of a spinophilin-GFP fusion protein, Bloom et al. have captured a remarkable polarization of

210 end resection using purified human proteins: Bloom helicase (BLM); DNA2 helicase/nuclease; Exonucleas

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

212 ormed two trials: one in autosomal recessive Bloom syndrome, in which a unique mutation of the BLM ge

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

214 Five paralogues (RecQ1, Bloom, Werner, RecQ4, and RecQ5) are found in human cell

215 human cells, when compared with the related Bloom syndrome RECQ helicase protein.

216 ECQ family: (1) the BLM subgroup (H. sapiens Bloom, D. melanogaster Dmblm, and Caenorhabditis elegans

217 cantly differ according to tumor size, Scarf-Bloom-Richardson grade, or Ki-67 expression.

218 one receptor, DNA ploidy, S phase, or Scarff-Bloom-Richardson score.

219 ectively, and graded according to the Scarff-Bloom-Richardson scale.

220 Here we introduce Sequence Bloom Trees (SBTs), a method for querying thousands of s

221 Arabidopsis slow growth suppressor 1 (Sgs1)/Bloom syndrome protein (BLM) homologs--as major barriers

222 g reads (BLESS), uses a single minimum-sized Bloom filter, and is also able to tolerate a higher fals

223 to the surface, increasing the fat and sugar Bloom formation.

224 s, xeroderma pigmentosum, Cockayne syndrome, Bloom syndrome, and Rothmund-Thomson syndrome.

225 xeroderma pigmentosum, Cockayne's syndrome, Bloom's syndrome and Werner's syndrome, have been linked

226 enetic disorders, including Werner Syndrome, Bloom Syndrome and Rothmund-Thomson Syndrome, exhibit ge

227 cancer or premature aging: Werner syndrome, Bloom syndrome, and Rothmund-Thomson syndrome.

228 d progeria syndrome (HGPS), Werner syndrome, Bloom syndrome, Cockayne syndrome, trichothiodystrophy,

229 We show that Bloom helicase (BLM) is degraded during adenovirus type

230 Bulk biochemical studies have shown that Bloom helicase (BLM) unfolds both intermolecular and int

231 t component of p53 function and suggest that Bloom Syndrome phenotype may in part be the result of th

232 ant role in DNA replication, suggesting that Bloom's syndrome may be the consequence of defective DNA

233 The Bloom syndrome (BS) protein, BLM, is a member of the Rec

234 The Bloom syndrome gene BLM encodes a RecQ DNA helicase, who

235 The Bloom syndrome gene, BLM, encodes a RecQ DNA helicase th

236 The Bloom syndrome helicase BLM and topoisomerase-IIbeta-bin

237 The Bloom syndrome patient (BLM) protein defective in the di

238 The Bloom's helicase ortholog, Sgs1, plays central roles to

239 The Bloom's syndrome gene (BLM) plays a pivotal role in the

240 The Bloom's syndrome gene product, BLM, belongs to the RecQ

241 The Bloom's syndrome helicase (BLM), mutations of which lead

242 The Bloom's syndrome helicase, BLM, is a member of the highl

243 Although the Bloom (BLM) syndrome helicase was also inhibited by a ci

244 encoding RecQ-like DNA helicases such as the Bloom and Werner syndrome genes, BLM and WRN, have been

245 sly identified G4 DNA helicases, such as the Bloom's helicase (BLM), FANCJ unwinds G4 substrates with

246 formation and chromatin loading of BLM (the Bloom syndrome helicase).

247 acting checkpoint helicase) and the BLM (the Bloom's syndrome protein) helicase decorate ultrafine hi

248 hat the RecQ family helicases encoded by the Bloom's and Werner's syndrome genes are likely to act in

249 nding activity on G-quadruplex (G4) DNA, the Bloom syndrome-associated helicase BLM is proposed to pa

250 nic stem (ES) cells, mutations in either the Bloom syndrome homologue (Blm) or the Recql5 genes resul

251 with a genetic background deficient for the Bloom's syndrome helicase, such heterozygous mutants seg

252 The latter are mutated, respectively, in the Bloom and Werner syndromes, whose manifestations include

253 1Y and K422R), observed earlier by us in the Bloom syndrome condition.

254 In the Bloom syndrome trial, by Fisher's exact test, statistica

255 In the Bloom syndrome trial, we genotyped 3,258 SNPs in 10 Jewi

256 n the Werner syndrome; BLM, deficient in the Bloom syndrome; and Drosophila melanogaster RecQ5b (dmRe

257 predisposition, results from defects in the Bloom's helicase (BLM) protein.

258 of DNA helicases, whose members include the Bloom's syndrome and the Werner's syndrome gene products

259 family of DNA helicases, which includes the Bloom's (BLM) and Werner's (WRN) syndrome gene products,

260 ng double-strand break repair, including the Bloom syndrome (BLM) helicase and exonuclease 1 (EXO1),

261 rosophila melanogaster mutants that lack the Bloom syndrome helicase.

262 WRN and for another RecQ family member, the Bloom syndrome protein (BLM).

263 Moreover, the Bloom's syndrome gene (BLM), discovered before WRN, is a

264 and mei-218 mutants; however, removal of the Bloom syndrome helicase (BLM) ortholog restored crossove

265 in mus309, which encodes the ortholog of the Bloom Syndrome helicase.

266 The product of the Bloom syndrome mutated gene, designated BLM, is a member

267 t lack DmBlm, the Drosophila ortholog of the Bloom syndrome protein, increases the percentage and ove

268 BLM and WRN, the products of the Bloom's and Werner's syndrome genes, are members of the

269 Mutation of the Bloom's syndrome (BS) gene, BLM, results in genomic inst

270 rotein complex stimulated the ability of the Bloom's syndrome gene product, BLM, to process Holliday

271 The conserved BTR complex, composed of the Bloom's syndrome helicase (BLM), topoisomerase IIIalpha,

272 Successful fork recovery depends on the Bloom's helicase BLM that participates in a larger prote

273 Here, we show that whereas either WRN or the Bloom syndrome helicase (BLM) stimulates DNA polymerase

274 nomic stability, perhaps in concert with the Bloom or Werner syndrome DNA helicases.

275 passage, forms a conserved complex with the Bloom's helicase (BLM, Sgs1 in budding yeast).

276 Mutations in Bloom helicase (BLM) lead to Bloom Syndrome (BS).

277 Mutations in BLM give rise to Bloom syndrome, a disease that is characterized by an el

278 which encodes a RecQ helicase, give rise to Bloom's syndrome, a disorder associated with cancer pred

279 Homozygous inactivation of BLM gives rise to Bloom's syndrome, a disorder associated with genomic ins

280 NA ligase I displayed a phenotype similar to Bloom's syndrome, being immunodeficient, growth retarded

281 Unfortunately Bloom-Richardson (BR) grade determined by pathologists c

282 em cell technology, we have generated viable Bloom mice that are prone to a wide variety of cancers.

283 uman RecQ helicase diseases, such as Werner, Bloom, and Rothmund-Thomson syndromes, are also related

284 sposition and/or shortened lifespan (Werner, Bloom, and Rothmund-Thomson syndromes).

285 binding protein RPA, and the Srs2 and Werner/Bloom helicases, but not Ku and ligase 4.

286 underpin early-onset cancers associated with Bloom's syndrome.

287 aracteristics of cells from individuals with Bloom's or Werner's syndrome.

288 ng of the gene defective in individuals with Bloom's syndrome has revealed a link between DNA helicas

289 BLM protein, inactivated in individuals with Bloom's syndrome, acts in combination with topoisomerase

290 c in primary fibroblasts from a patient with Bloom syndrome than in normal human fibroblasts.

291 BLM and WRN are mutated in patients with Bloom's syndrome and Werner's syndrome respectively.

292 chromatid exchanges (SCEs) and patients with Bloom's syndrome develop a broad spectrum of early-onset

293 In cells from persons with Bloom syndrome the localization of PML is unperturbed, w

294 The genomic instability of persons with Bloom's syndrome (BS) features particularly an increased

295 eproductive system, and bone, and those with Bloom syndrome display more limited features of aging, i