ライフサイエンスコーパス: premature aging

1 opoietic system from changes associated with premature aging.

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

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

4 tionship between chromosomal instability and premature aging.

5 cular dystrophy, dilated cardiomyopathy, and premature aging.

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

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

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

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

10 e, and other abnormalities characteristic of premature aging.

11 associated with cancer predisposition and/or premature aging.

12 B-cell progenitor populations reminiscent of premature aging.

13 ated with chromosomal instability as well as premature aging.

14 nome instability, cancer susceptibility, and premature aging.

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

16 racterized by extensive clinical features of premature aging.

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

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

19 e genetic disorder characterized by dramatic premature aging.

20 nd increasing glucose levels, reminiscent of premature aging.

21 53+/- mice display cancer susceptibility and premature aging.

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

23 eficiency-associated embryonic lethality and premature aging.

24 s are rare genetic diseases characterized by premature aging.

25 autosomal recessive disease that results in premature aging.

26 pair defects can cause phenotypes resembling premature aging.

27 lti-system degenerative phenotype resembling premature aging.

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

29 ase characterized by genomic instability and premature aging.

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

31 symptoms that include neurodegeneration and premature aging.

32 sensitivity, developmental abnormalities and premature aging.

33 age-related dysfunction in a mouse model of premature aging.

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

35 ely, results in phenotypes characteristic of premature aging.

36 human disease with manifestations resembling premature aging.

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

38 ts, namely cancer, neurological disease, and premature aging.

39 autosomal recessive disease characterized by premature aging.

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

41 ensitivity, developmental abnormalities, and premature aging.

42 mutation leads to Werner syndrome resembling premature aging.

43 human genetic disorder with many features of premature aging.

44 mutator mouse is a well-established model of premature aging.

45 recessive disease, which is characterized by premature aging.

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

47 gressive loss of mitochondrial integrity and premature aging.

48 hritis features was not found accelerated in premature aging.

49 n Werner syndrome of genomic instability and premature aging.

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

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

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

53 cer, immunodeficiency, genetic disorders and premature aging.

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

55 ent, neurological degeneration and segmental premature aging.

56 Mice deficient in Mpv17 show signs of premature aging.

57 ut mice are prone to genomic instability and premature aging.

58 ereby contributing to therapy resistance and premature aging.

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

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

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

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

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

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

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

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

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

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

69 The premature aging and cancer-prone disease Werner syndrome

70 The premature aging and cancer-prone disease Werner syndrome

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

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

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

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

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

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

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

78 ultrarare and fatal disease with features of premature aging and cardiovascular diseases (atheroscler

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

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

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

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

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

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

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

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

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

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

89 mark features of HR insufficiency, including premature aging and hypersensitivity to PARPi.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 nA homolog, OOC-5, rescues the sterility and premature aging caused by a null mutation in the single

112 Here we evaluated whether premature aging caused by accumulation of mitochondrial

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

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

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

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

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

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

119 ary feature of Werner syndrome (WS), a human premature aging disease caused by mutations in the gene

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

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

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

123 or ZMPSTE24 that prevent cleavage cause the premature aging disease Hutchinson-Gilford progeria synd

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

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

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

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

128 The premature aging disease Hutchinson-Gilford Progeria Synd

129 orders known as laminopathies, including the premature aging disease Hutchinson-Gilford progeria synd

130 hinson-Gilford Progeria Syndrome (HGPS) is a premature aging disease in children that leads to early

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 hinson-Gilford progeria syndrome (HGPS) is a premature aging disorder characterized by accelerated ca

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

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

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

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

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

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

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

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

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

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

160 icing in exon 11 of the LMNA gene causes the premature aging disorder Hutchinson-Gilford Progeria Syn

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

162 A cause degenerative disorders including the premature aging disorder Hutchinson-Gilford progeria, bu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 Premature aging disorders provide an opportunity to stud

179 pulmonary fibrosis; they are the most common premature aging disorders.

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

181 lve this, we generated novel mouse models of premature aging, driven by CDGSH iron sulfur domain 2 (

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

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

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

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

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

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

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

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

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

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

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

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

194 Premature aging in Hutchinson-Gilford progeria syndrome

195 Premature aging in Hutchinson-Gilford progeria syndrome

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

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

198 eractivity results in genome instability and premature aging in mice (Kopp et al., 2019).

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

200 Deleting a long noncoding RNA drives premature aging in mice.

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

202 e (HGPS) is a fatal disease characterized by premature aging in which young children fail to thrive a

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

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

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

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

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

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

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

210 tutive Cisd2-deficient mice display signs of premature aging, including testicular atrophy, reduced L

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

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

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

214 The premature aging is not associated with increased cellula

215 Premature aging is studied in a genetically modified mou

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

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

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

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

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

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

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

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

224 tudied intensively because the mechanisms of premature aging may lead to a better understanding of no

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

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

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

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

229 Therefore, normal/premature aging of BM niches promotes myeloid expansion

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

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

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

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

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

235 resilience against neurological diseases or premature aging of the brain.

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

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

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

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

240 ocused on lowering cancer risk by preventing premature aging or promoting healthy aging.

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

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

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

244 subjects sharing these mutations revealed a premature aging phenotype as a previously unrecognized f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

265 However, mice with Cisd2 deletion (and thus premature aging) restricted to either LCs or SCs were pr

266 helicase, deficient in the cancer-prone and premature aging Rothmund-Thomson syndrome, physically an

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

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

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

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

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

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

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

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

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

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

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

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

279 with Hutchinson-Gilford progeria syndrome, a premature aging syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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