ライフサイエンスコーパス: premature aging

1 es, including low insulin, hypoglycemia, and premature aging.

2 e, and other abnormalities characteristic of premature aging.

3 associated with cancer predisposition and/or premature aging.

4 B-cell progenitor populations reminiscent of premature aging.

5 ated with chromosomal instability as well as premature aging.

6 gressive loss of mitochondrial integrity and premature aging.

7 nome instability, cancer susceptibility, and premature aging.

8 me (HGPS) is the most dramatic form of human premature aging.

9 racterized by extensive clinical features of premature aging.

10 mplicated in cellular senescence, aging, and premature aging.

11 de in the understanding of the mechanisms of premature aging.

12 e genetic disorder characterized by dramatic premature aging.

13 nd increasing glucose levels, reminiscent of premature aging.

14 53+/- mice display cancer susceptibility and premature aging.

15 rmorphic (p53+/m) mice display phenotypes of premature aging.

16 eficiency-associated embryonic lethality and premature aging.

17 s are rare genetic diseases characterized by premature aging.

18 autosomal recessive disease that results in premature aging.

19 pair defects can cause phenotypes resembling premature aging.

20 HSCs and progenitor cells, and in preventing premature aging.

21 s, or peripheral nerves or cause features of premature aging.

22 ase characterized by genomic instability and premature aging.

23 s can be used to predict lifespan and detect premature aging.

24 symptoms that include neurodegeneration and premature aging.

25 sensitivity, developmental abnormalities and premature aging.

26 eral aspects of genomic stability, also show premature aging.

27 n Werner syndrome of genomic instability and premature aging.

28 ely, results in phenotypes characteristic of premature aging.

29 human disease with manifestations resembling premature aging.

30 with syndromes of genomic instability and/or premature aging.

31 autosomal recessive disease characterized by premature aging.

32 er initiation or progression or in normal or premature aging.

33 thymus in human naive T cell homeostasis and premature aging.

34 ensitivity, developmental abnormalities, and premature aging.

35 mutation leads to Werner syndrome resembling premature aging.

36 human genetic disorder with many features of premature aging.

37 e, the phenotype of which is a caricature of premature aging.

38 utosomal recessive disorder characterized by premature aging.

39 syndrome, a disease with symptoms resembling premature aging.

40 ed disease with clinical symptoms resembling premature aging.

41 ng and prolongs lifespan in a mouse model of premature aging.

42 nts display signs that in some ways resemble premature aging.

43 cer, immunodeficiency, genetic disorders and premature aging.

44 sembly checkpoint, which in turn can lead to premature aging.

45 ent, neurological degeneration and segmental premature aging.

46 Mice deficient in Mpv17 show signs of premature aging.

47 ereby contributing to therapy resistance and premature aging.

48 tential, stem cell exhaustion, alopecia, and premature aging.

49 KO (Casp2(-/-)) mice show characteristics of premature aging.

50 tionship between chromosomal instability and premature aging.

51 cular dystrophy, dilated cardiomyopathy, and premature aging.

52 a truncated form of lamin A associated with premature aging.

53 m of diseases that share certain features of premature aging.

54 degenerative diseases, diabetes, cancer, and premature aging.

55 rized by lowered respiratory chain activity, premature aging, age-related motor deficits as well as a

56 ne, accumulate ERCs more rapidly, leading to premature aging and a shorter life span.

57 c disorder that is characterized by dramatic premature aging and accelerated cardiovascular disease.

58 insights into the mechanisms responsible for premature aging and also shed light on the role of lamin

59 autosomal recessive disorder associated with premature aging and cancer predisposition caused by muta

60 planation on how SPRTN deficiency causes the premature aging and cancer predisposition disorder Ruijs

61 tions affecting human RecQ proteins underlie premature aging and cancer predisposition syndromes, inc

62 lity with some phenotypic characteristics of premature aging and cancer predisposition.

63 is associated with chromosomal instability, premature aging and cancer predisposition.

64 The first three of are associated with premature aging and cancer prone syndromes, but the latt

65 ations in WRN are found in patients with the premature aging and cancer susceptibility syndrome known

66 The premature aging and cancer-prone disease Werner syndrome

67 The premature aging and cancer-prone disease Werner syndrome

68 The premature aging and cancer-prone diseases Werner and Blo

69 elicase family, loss of which results in the premature aging and cancer-prone disorder, Werner syndro

70 Werner syndrome is a premature aging and cancer-prone hereditary disorder cau

71 es are defective in diseases associated with premature aging and cancer.

72 nd bring insight to the mechanisms that link premature aging and cancer.

73 are mutated in human diseases manifesting in premature aging and cancer.

74 adiation from the sun can result in sunburn, premature aging and carcinogenesis, but the mechanism re

75 iduals and patients with genetic diseases of premature aging and compared their sequences to each oth

76 disorder that is characterized by segmental premature aging and death between 7 and 20 years of age

77 s, yeast organisms undergo an altruistic and premature aging and death program, mediated in part by s

78 ological alterations that invariably lead to premature aging and death.

79 rdiovascular system during physiological and premature aging and discusses the mechanisms underlying

80 RN, is a hereditary disease characterized by premature aging and elevated cancer incidence.

81 Sirt1-deficient mice exhibited profound premature aging and enhanced acetylation of histone H4 o

82 ecessive disorder in humans characterized by premature aging and genetic instability.

83 The WRN gene, defective in the premature aging and genome instability disorder Werner s

84 S) is an inherited disorder characterized by premature aging and genomic instability.

85 rder, Werner syndrome (WS), distinguished by premature aging and genomic instability; all are reporte

86 drome, in which patients exhibit features of premature aging and increased cancer.

87 Werner syndrome is associated with premature aging and increased risk of cancer.

88 s congenita (DC), a disease characterized by premature aging and increased tumor susceptibility.

89 uman autosomal recessive disease that mimics premature aging and is associated with genetic instabili

90 yndrome (WS) is characterized by features of premature aging and is caused by loss of the RecQ helica

91 hat is characterized by multiple features of premature aging and largely affects tissues of mesenchym

92 o increases the lifespan of a mouse model of premature aging and provides health benefits to chronolo

93 l diseases, including those with features of premature aging and skeletal abnormalities.

94 he HSC and MPP phenotypes are reminiscent of premature aging and stressed hematopoiesis, and indeed p

95 have a blood phenotype with similarities to premature aging and to human diseases of myelodysplastic

96 ince several human diseases characterized by premature aging and/or cancer have been genetically link

97 lay of factors controlling genome stability, premature aging, and cancer.

98 ome characterized by skin hyperpigmentation, premature aging, and increased skin cancer, is caused by

99 onal loss has been linked to carcinogenesis, premature aging, and neurodegeneration.

100 e diseases characterized by abnormal growth, premature aging, and predisposition to malignancies.

101 and developmental abnormalities and dramatic premature aging, and their cells are hypersensitive to o

102 ip between progerias--diseases that resemble premature aging--and the normal aging process has been a

103 ndelian progeroid syndrome in which signs of premature aging are associated with genomic instability

104 ner syndrome (WS), which is characterized by premature aging as well as genomic and telomeric instabi

105 taining genome integrity and thus preventing premature aging, cancer and many other human diseases by

106 racterized by the early onset of symptoms of premature aging, cancer, and genomic instability.

107 ria syndrome is a rare inherited disorder of premature aging caused by mutations in LMNA or Zmpste24

108 epletion of Foxp1 in bone marrow MSCs led to premature aging characteristics, including increased bon

109 racterized by aberrant telomere maintenance, premature aging, chromosomal rearrangements, and predisp

110 Cockayne syndrome (CS) is a premature aging condition characterized by sensitivity t

111 Cockayne syndrome is a premature aging disease associated with numerous develop

112 ford progeria syndrome (HGPS) is a childhood premature aging disease caused by a spontaneous point mu

113 Werner syndrome (WS) is a rare human premature aging disease caused by mutations in the gene

114 are a hallmark of premature aging.HGPS is a premature aging disease caused by mutations in the nucle

115 The segmental premature aging disease Hutchinson-Gilford Progeria (HGP

116 e mutant form of lamin A responsible for the premature aging disease Hutchinson-Gilford progeria synd

117 gene encoding nuclear lamin A (LA) cause the premature aging disease Hutchinson-Gilford Progeria Synd

118 rous human diseases, including the segmental premature aging disease Hutchinson-Gilford progeria synd

119 The premature aging disease Hutchinson-Gilford Progeria Synd

120 es the ZMPSTE24 cleavage site, underlies the premature aging disease Hutchinson-Gilford Progeria Synd

121 The protein mutated in the premature aging disease known as the Werner syndrome is

122 amin processing (laminopathies), such as the premature aging disease progeria and metabolic disorders

123 rd progeria syndrome (HGPS) is a devastating premature aging disease resulting from a mutation in the

124 progeria syndrome is an ultrarare segmental premature aging disease resulting in early death from he

125 hinson-Gilford progeria syndrome (HGPS) is a premature aging disease that is frequently caused by a d

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

127 The cancer-prone and premature aging disease Werner syndrome is due to loss o

128 , a DNA helicase and exonuclease, causes the premature aging disease Werner syndrome.

129 ford progeria syndrome (HGPS), a devastating premature aging disease, is caused by a point mutation i

130 the human A-type lamin gene (LMNA) cause the premature aging disease, progeria.

131 s and from patients with progeria, a genetic premature aging disease.

132 with cancer and laminopathies, including the premature-aging disease Hutchinson-Gilford progeria synd

133 nance mechanisms leads to the development of premature aging diseases, such as dyskeratosis congenita

134 Werner syndrome (WS), an autosomal recessive premature aging disorder associated with cancer predispo

135 Cockayne syndrome (CS) is a human premature aging disorder associated with neurological an

136 Cockayne syndrome (CS) is a human premature aging disorder associated with severe developm

137 d progeria syndrome (HGPS) is a severe human premature aging disorder caused by a lamin A mutant name

138 Werner syndrome (WS) is a premature aging disorder caused by WRN protein deficienc

139 Werner Syndrome is a premature aging disorder characterized by chromosomal in

140 Werner syndrome (WS) is a human premature aging disorder characterized by chromosomal in

141 Cockayne syndrome (CS) is a premature aging disorder characterized by developmental

142 tchinson-Gilford progeria syndrome (HGPS), a premature aging disorder characterized by excessive athe

143 Werner syndrome is a hereditary premature aging disorder characterized by genome instabi

144 Werner syndrome is a hereditary premature aging disorder characterized by genomic instab

145 Werner Syndrome is a premature aging disorder characterized by genomic instab

146 Cockayne syndrome (CS) is a premature aging disorder characterized by photosensitivi

147 Werner syndrome (WS) is a human premature aging disorder characterized by the early onse

148 Werner syndrome is a human premature aging disorder displaying cellular defects ass

149 rin, the lamin A isoform responsible for the premature aging disorder Hutchinson-Gilford progeria syn

150 Werner syndrome (WS) is the hallmark premature aging disorder in which affected humans appear

151 Werner syndrome (WS) is a genetic premature aging disorder in which patients appear much o

152 The progress made on the premature aging disorder Progeria is a shining example o

153 cell datasets, addressing the diagnosis of a premature aging disorder using images of cell nuclei, as

154 The human premature aging disorder Werner syndrome (WS) is associa

155 f cancer and aging, and is a hallmark of the premature aging disorder Werner syndrome (WS).

156 rner syndrome helicase (WRN), mutated in the premature aging disorder Werner syndrome.

157 Werner syndrome (WS) is a premature aging disorder where the affected individuals

158 Hutchinson Gilford progeria syndrome is a premature aging disorder wherein a mutant version of lam

159 hinson-Gilford progeria syndrome (HGPS) is a premature aging disorder, commonly caused by a point mut

160 Werner syndrome (WS) is a premature aging disorder, displaying defects in DNA repl

161 Werner protein (WRN) and manifest as a rare premature aging disorder, Werner syndrome.

162 syndrome (HGPS) is a rare, invariably fatal premature aging disorder.

163 the pathogenesis of Werner syndrome (WS), a premature-aging disorder.

164 ll also discuss the clinical features of the premature aging disorders associated with RecQ helicase

165 Premature aging disorders provide an opportunity to stud

166 e prelamin A results in progeria and related premature aging disorders.

167 autosomal recessive disease characterized by premature aging, elevated genomic instability and increa

168 limit breakdown of elastin, a major cause of premature aging, following UVB exposure to human reconst

169 ), a genetic disease that is associated with premature aging for children.

170 c, autosomal dominant syndrome that involves premature aging, generally leading to death at approxima

171 ome is an inherited disease characterized by premature aging, genetic instability and a high incidenc

172 disease whose phenotype includes features of premature aging, genetic instability, and an elevated ri

173 yndrome is a human disorder characterized by premature aging, genomic instability, and abnormal telom

174 Werner Syndrome (WS) is characterized by premature aging, genomic instability, and cancer.

175 particularly HGPS, the most dramatic form of premature aging, have contributed to our knowledge of fu

176 me biogenesis and activity are a hallmark of premature aging.HGPS is a premature aging disease caused

177 PS-modeled LamC mutations induced premature aging in adult flight muscles, including decre

178 ry Tangier fibroblasts were characterized by premature aging in culture and were associated with less

179 sms responsible for the rapid progression of premature aging in HGPS patients.

180 Premature aging in Hutchinson-Gilford progeria syndrome

181 that phosphate toxicity is the main cause of premature aging in klotho(-/-) mice.

182 owever, the molecular signals underlying the premature aging in lungs, and whether SIRT1 protects aga

183 ruption of TFAM results in heart failure and premature aging in mice.

184 n genomic instability syndrome that includes premature aging in some of the patients.

185 ure commonly associated with infertility and premature aging in women.

186 n failure, a common cause of infertility and premature aging in women.

187 may contribute to the aging process and the premature aging in WS.

188 Mutation of SGS1 is shown to cause premature aging in yeast mother cells on the basis of a

189 ed lifespans and display various symptoms of premature aging including sarcopenia, cataracts, less su

190 pathophysiological processes consistent with premature aging including severe atrophy of tissues.

191 , and morphological features consistent with premature aging, including kyphosis, uncoordinated movem

192 mice display signs of growth retardation and premature aging, including low birth weight, failure to

193 ility, and misregulation of BER is linked to premature aging, increased rate of mutagenesis, and canc

194 logies that include developmental disorders, premature aging, infertility and predisposition to cance

195 rome (HGPS) and restrictive dermopathy (RD), premature aging is linked to accumulation of DNA double-

196 Premature aging is studied in a genetically modified mou

197 e disease that results in what appears to be premature aging, is caused by the production of a mutant

198 pic calcifications and significantly rescues premature aging-like features of Fgf-23-/- mice, resulti

199 mice by feeding with a high-phosphate diet, premature aging-like features reappeared, clearly sugges

200 ndicate a novel role of Fgf-23 in developing premature aging-like features through regulating vitamin

201 tho(-/-)) strain resulted in amelioration of premature aging-like features.

202 tened life span of the animals; and multiple premature aging-like phenotypes, including a reduction i

203 l and morphological features consistent with premature aging-like phenotypes, including kyphosis, sev

204 c condition of young adults characterized by premature aging, limited replicative capacity of cells i

205 sgs1 and srs2 cells senesce due to apparent premature aging, most likely involving the accumulation

206 in the prevention of human diseases, such as premature aging, neurodegenerative diseases, and cancer.

207 a large number of human diseases, including premature aging, neurodegenerative disorders, cardiovasc

208 man disorder characterized by pathologies of premature aging, neurological abnormalities, sensorineur

209 r, and that UC can be viewed as resulting in premature aging of colorectal epithelial cells.

210 We show that XLF deficiency leads to premature aging of hematopoietic stem cells (HSCs), meas

211 We propose that premature aging of HSCs, together with previously report

212 HDV infection, the largest to date, revealed premature aging of immune cells and impaired T-cell func

213 To test whether premature aging of mammary epithelial stem cells would h

214 Although the accelerated atherosclerosis and premature aging of the cardiovascular system in patients

215 otably, this depletion mitigated TBI-induced premature aging of the hematopoietic system and rejuvena

216 Persons with Werner syndrome displays premature aging of the skin, vasculature, reproductive s

217 affect Leydig cell function, likely causing premature aging of the testes and impaired liver metabol

218 Despite their rarity, diseases of premature aging, or "progeroid" syndromes, have provided

219 ic pathology (e.g., early onset arthropathy, premature aging, ovulation, late onset of puberty, and a

220 onse to catabolic stress may account for the premature aging phenotype and apoptosis of OA chondrocyt

221 proof of principle for the correction of the premature aging phenotype in individuals with HGPS.

222 vestigate the molecular mechanism underlying premature aging phenotype in Polg mutant mice.

223 tDNA deletions as a driving force behind the premature aging phenotype of mitochondrial mutator mice,

224 We use three mouse models, namely, a premature aging phenotype, a mature aging phenotype, and

225 tosomal recessive disease characterized by a premature aging phenotype, genomic instability, and a dr

226 DNA polymerase gamma, was shown to develop a premature aging phenotype, including sarcopenia, cardiom

227 yndrome is an inherited disease displaying a premature aging phenotype.

228 tion, developmental growth retardation and a premature aging phenotype.

229 idative response as a key contributor to the premature aging phenotype.

230 y transmitted mtDNA mutations can cause mild premature aging phenotypes also in mice with a wild-type

231 frequency at existing sites even before the premature aging phenotypes appear.

232 GC-1alpha expression is able to improve some premature aging phenotypes in the mutator mice without r

233 bits DSB repair, thereby contributing to the premature aging phenotypes observed in progeria arising

234 Mutations in DNA repair genes and premature aging phenotypes they cause have been reviewed

235 ) and Bloom (BLM), respectively, and display premature aging phenotypes.

236 Consistent with these premature-aging phenotypes, Cdc14b-deficient cells accum

237 of human skin to solar UV radiation leads to premature aging (photoaging) and skin cancer.

238 gical aging and solar UV irradiation-induced premature aging (photoaging).

239 o, a gene described as being associated with premature aging process.

240 t to delay aging and that when mutated cause premature aging (progeria).

241 WS is characterized by the early onset of premature aging signs and a high incidence of sarcomas.

242 mply that the genomic instability, segmental premature aging symptoms, and cancer predisposition asso

243 D-EDMD) and Hutchinson-Gilford progeria, the premature aging syndrome (HGPS).

244 HGPS) is an extremely rare, fatal, segmental premature aging syndrome caused by a mutation in LMNA th

245 drome is an extremely rare, fatal, segmental premature aging syndrome caused by a mutation in LMNA yi

246 Werner syndrome (WS) is a premature aging syndrome caused by mutations in the WS g

247 Dyskeratosis congenita is a premature aging syndrome characterized by muco-cutaneous

248 g and progressive bone marrow failure in the premature aging syndrome dyskeratosis congenita.

249 nuclear structural protein lamin A cause the premature aging syndrome Hutchinson-Gilford progeria (HG

250 Based on observations in the premature aging syndrome Hutchinson-Gilford progeria, we

251 dysfunction elicits a classical Werner-like premature aging syndrome typified by premature death, ha

252 e many human diseases, including progeria, a premature aging syndrome, whereas LMNB1 duplication caus

253 ogerin, a mutated lamin A, causes the severe premature-aging syndrome Hutchinson-Gilford progeria (HG

254 WS) is the canonical adult human progeroid ('premature aging') syndrome.

255 to human diseases ranging from BM failure to premature aging syndromes and cancer.

256 Mutations in lamins cause premature aging syndromes in humans, including the Hutch

257 is associated with cancer predisposition and premature aging syndromes in humans.

258 he IGF-I-Akt-56K pathway can protect against premature aging syndromes in mammals.

259 er of DNA repair abnormalities are linked to premature aging syndromes, and these are associated with

260 referred to as laminopathies, which include premature aging syndromes, lipodystrophy, and striated m

261 lamin A cause a number of diseases including premature aging syndromes, muscular dystrophy, and cardi

262 o genome instability, heritable cancers, and premature aging syndromes.

263 ch as muscular dystrophies and some types of premature aging syndromes.

264 hies, cardiomyopathies, lipodystrophies, and premature aging syndromes.

265 nge from muscular dystrophy to neuropathy to premature aging syndromes.

266 eatures include short stature, hearing loss, premature aging, telangiectasia, neurodegeneration, and

267 s, pronounced cellular senescence, and rapid premature aging that increases with successive generatio

268 lamins and devastating diseases ranging from premature aging to cancer.

269 Computational simulations confirm that premature aging together with a relatively high mutation

270 highlight recent advances in the biology of premature aging uncovered in Hutchinson-Gilford progeria

271 cQ helicase, the WRN protein involved in the premature aging Werner syndrome, do not exhibit the gene

272 erized by an elevated incidence of cancer or premature aging: Werner syndrome, Bloom syndrome, and Ro

273 11) display both increased tumorigenesis and premature aging, yet molecular mechanisms underlying the