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 helicase (BLM) and its orthologs are essential for

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

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

9 Bloom reduces the shelf-life of chocolate and affects it

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

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

12 Bloom syndrome (BS) is a hereditary disorder characteriz

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

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

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

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

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

18 Bloom syndrome (BS) is characterized by genomic instabil

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

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

21 Bloom syndrome and Werner syndrome are genome instabilit

22 Bloom syndrome confers strong predisposition to malignan

23 Bloom syndrome is a disorder associated with genomic ins

24 Bloom syndrome is a disorder of profound and early cance

25 Bloom syndrome is a familial genetic disorder associated

26 Bloom syndrome is a rare autosomal disorder characterize

27 Bloom syndrome is a rare disorder associated with cancer

28 Bloom syndrome is a rare, autosomal recessive inherited

29 Bloom Syndrome is an autosomal recessive cancer-prone di

30 Bloom syndrome is an autosomal recessive disorder associ

31 Bloom syndrome is an autosomal recessive disorder caused

32 Bloom syndrome patients have a strong predisposition to

33 Bloom Syndrome, a rare human disorder characterized by g

34 Bloom syndrome, characterized by a predisposition to can

35 Bloom value was also significantly higher in frog skin g

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

37 Bloom's syndrome (BLM) helicase together with exonucleas

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

54 Bloom's syndrome is a genetic disorder characterized by

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

56 Bloom's syndrome is a rare autosomal recessive disorder

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

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

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

60 Bloom-derived organic matter, much of it occurring as po

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

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

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

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

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

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

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

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

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

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

71 otein complex of topoisomerase III alpha and Bloom helicase.

72 Fanconi anemia and Bloom syndrome are genomic instability syndromes caused

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

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

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

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

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

78 ispositions, such as DICER1, Li-Fraumeni and Bloom syndrome, as well as Fanconi anemia.

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

80 (A-T), Nijmegen breakage syndrome (NBS) and Bloom syndrome (BS) are clinically distinct, chromosome

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

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

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

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

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

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

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

88 predisposition syndromes Werner syndrome and Bloom syndrome.

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

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

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

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

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

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

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

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

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

98 Werner and Bloom syndromes are genetic RecQ helicase disorders char

99 Werner and Bloom syndromes are human diseases characterized by prem

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

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

102 ted to mitigate this component of Werner and Bloom syndromes.

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

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

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

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

107 Werner Syndrome (WS) and Bloom Syndrome (BS) are disorders of DNA damage repair c

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

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

110 on unless destabilized by helicases, such as Bloom helicase (BLM).

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

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

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

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

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

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

117 Upon DNA unwinding by Bloom (BLM) or Werner (WRN) helicase, RPA directs the DN

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

167 ial for genome integrity and is deficient in Bloom syndrome (BS), a rare genetic disease characterize

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

188 erited mutations in RecQ helicases result in Bloom Syndrome (BLM mutation), Werner Syndrome (WRN muta

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

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

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

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

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

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

195 methods-including Vari, Rainbowfish, Mantis, Bloom Filter Trie, the method of Almodaresi et al. and M

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

197 %Su and 75%St+25%Su samples showed a minimum Bloom formation, probably due to its dense microstructur

198 abilistic data structure called a multiindex Bloom Filter (miBF), which can store multiple spaced see

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

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

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

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

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

204 LM defects represent the underlying cause of Bloom Syndrome, a rare genetic disorder that is marked b

205 sister chromatid exchange characteristic of Bloom's syndrome.

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

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

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

209 microstructure and the highest percentage of Bloom was observed.

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

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

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

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

214 accurate lossy compression based on a set of Bloom filters.

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

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

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

218 BLM, defects in which cause the cancer-prone Bloom's Syndrome.

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

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

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

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

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

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

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

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

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

228 f biopsy specimens: histological type, Scarf-Bloom, Ki67, and p53 in the infiltrating component as we

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

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

231 Recently, the Sequence Bloom Tree (SBT) and its derivatives were proposed as a

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

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

234 using Drosophila as a model system to study Bloom Syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

264 1Y and K422R), observed earlier by us in the Bloom syndrome condition.

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

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

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

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

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

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

271 rosophila melanogaster mutants that lack the Bloom syndrome helicase.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

292 anism and was reported to be associated with Bloom syndrome (BS) and cancer.

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

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

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

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

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

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

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

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