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1 rtic vascular smooth muscle cells from these progeroid animals had an impaired capacity to inhibit va
2 iffer subendothelial extracellular matrix in progeroid aortae, and ultrasound assessment of live HGPS
3  patients who had severe MAD associated with progeroid appearance and generalized lipodystrophy.
4 poatrophy and cutis laxa are the basis for a progeroid appearance.
5                     We also found that these progeroid cells exhibited nuclear foci of xeroderma pigm
6 camptothecin were efficiently removed in the progeroid cells.
7 A foci colocalized with the DSB sites in the progeroid cells.
8 ltraviolet-sensitive syndrome and the severe progeroid Cockayne syndrome.
9 ients with Werner syndrome (WS), a segmental progeroid condition with a high incidence of cancer, and
10  expression and alleviates the severity of a progeroid disease by increasing RNR activity.
11 reveal abnormal TP63 RT as an early event in progeroid disease progression, and suggest TP63 gene reg
12 ly of DNA helicases, have been linked to the progeroid disease Rothmund-Thomson Syndrome.
13 min A accumulates in cells, causing a severe progeroid disease, restrictive dermopathy (RD).
14 gy of a protein at the center of devastating progeroid diseases.
15 a osteodysplastica is a hereditary segmental progeroid disorder affecting skin, connective tissues, a
16               Werner syndrome (WS) is a rare progeroid disorder characterized by genomic instability,
17              Werner Syndrome (WS) is a human progeroid disorder characterized by genomic instability.
18 tations instead cause the neurodevelopmental progeroid disorder Cockayne syndrome, but little is know
19 fective in the autosomal recessive segmental progeroid disorder Cockayne syndrome.
20 ow that mouse models of Cockayne syndrome, a progeroid disorder resulting from a defect in the transc
21 helicase WRN protein causes the cancer-prone progeroid disorder Werner syndrome (WS).
22                               The segmental, progeroid disorder Werner syndrome results from loss of
23 ) has previously been shown to cause a human progeroid disorder, Nestor-Guillermo progeria syndrome (
24                                A more severe progeroid disorder, restrictive dermopathy (RD), is caus
25  syndrome (WS) is a rare autosomal recessive progeroid disorder.
26 athway mutations cause neurodegenerative and progeroid disorders (xeroderma pigmentosum (XP), Cockayn
27                                      Several progeroid disorders are caused by mutations that lead to
28                                              Progeroid disorders overlapping with De Barsy syndrome (
29 th farnesylated prelamin A and cause related progeroid disorders.
30 might be useful for treating LMNA-associated progeroid disorders.
31 Gilford progeria syndrome (HGPS) and related progeroid disorders.
32 stematically compared liver from 5-month-old progeroid Ercc1(-/Delta) mice to old (24-36-month-old) w
33  The affected individuals had short stature, progeroid facial features, a hypoplastic nose, xeroderma
34         CGL2 patients display characteristic progeroid features and suffer from type 2 diabetes, insu
35     Two of the girls had pronounced neonatal progeroid features and were initially diagnosed with Wie
36 ncommon autosomal recessive disease in which progeroid features are associated with genetic instabili
37  mice with reduced life span and accelerated progeroid features are indistinguishable from age-matche
38 ycle is perturbed and this might explain the progeroid features of the POLG mutator mouse.
39   We conclude that in line with the observed progeroid features, CGL2 patients exhibit significant ep
40 ogressive aneuploidy along with a variety of progeroid features, including short lifespan, cachectic
41 OMM7 can cause severe growth retardation and progeroid features.
42 n autosomal-dominant form of cutis laxa with progeroid features.
43 n inherited neurodevelopmental disorder with progeroid features.
44 identify base-editor-modified and unmodified progeroid fibroblasts from a heterogeneous population, v
45 rganismal aging in established long-lived or progeroid genetic models.
46 e dietary-restriction-like therapy for human progeroid genome instability syndromes and possibly neur
47 ansferase, which ranked as a top hit in both progeroid hMPC models.
48 c analyses of isogenic young, senescent, and progeroid human mesenchymal progenitor cells (hMPCs), we
49 nd genetic clearance of senescent cells from progeroid INK-ATTAC mice prevents lipodystrophy.
50 lerated in individuals with Down syndrome, a progeroid-like condition.
51 uffer from partial embryonic lethality and a progeroid-like phenotype.
52                    Werner syndrome (WS) is a progeroid-like syndrome caused by WRN gene mutations.
53                The Lmna null (Lmna(-/-)) and progeroid LmnaDelta9 mutant mice are models for AD-EDMD
54                               As both WT and progeroid mice aged, NF-kappaB was activated stochastica
55                                Zmpste24(-/-) progeroid mice also developed severe fibrosis-unrelated
56        Here we show that MDSPCs from old and progeroid mice are defective in proliferation and multil
57      Importantly, depletion of Pak2 in BubR1 progeroid mice attenuated the onset of aging-associated
58 SPCs, isolated from young wild-type mice, to progeroid mice confer significant lifespan and healthspa
59   The similarities between HGPS patients and progeroid mice reported here strongly suggest that defec
60                However, chronic treatment of progeroid mice with beta(3)-AR agonist decreases prematu
61 ger of EndMT, and treatment of VSMC-specific progeroid mice with SIS3 alleviated the aortic phenotype
62 ian and maximal remaining lifespans of these progeroid mice, strongly retarding numerous aspects of a
63 -associated hallmarks and extend lifespan in progeroid mice.
64 dy (mAb) improved health span in a strain of progeroid mice.
65 ssues from naturally aged and Ercc1(-/Delta) progeroid mice.
66 ECs, prevents exacerbated atherosclerosis in progeroid mice.
67 ayer and decreased atherosclerosis burden in progeroid mice.
68 90 inhibitor reduces age-related symptoms in progeroid mice.
69 hosphate inhibited vascular calcification in progeroid mice.
70  the age-related symptoms and pathologies of progeroid mice.
71 asured the activation of NF-kappaB in WT and progeroid model mice.
72 , the intima of ubiquitous and VSMC-specific progeroid models at the onset of atherosclerosis present
73               Here we show that in the BubR1 progeroid mouse background, INK-ATTAC removes p16(Ink4a)
74                        Clearance of SCs in a progeroid mouse model using a transgenic approach delays
75             Atherosclerotic lesions in these progeroid mouse models, but not in EC- and myeloid-speci
76 es similar to that of BubR1H/H mice, several progeroid pathologies were attenuated in severity, which
77 ing various cancers, congenital defects, and progeroid pathologies.
78            Moreover, the RT abnormalities in progeroid patients were associated with altered isoform
79 f mitochondrial DNA (mtDNA) deletions in the progeroid phenotype of exonuclease-deficient DNA polymer
80 expression, in contrast with the ameliorated progeroid phenotype of HGPSrev-SM22alpha-Cre mice.
81 n in the spotlight of aging research because progeroid phenotypes are associated with SIRT6 deficienc
82 ncreased mtDNA mutation levels contribute to progeroid phenotypes came from the mtDNA mutator mouse.
83 egulation of proteases potentially linked to progeroid phenotypes in CS, and our results suggest resc
84 thologies induced by DSBs, and the segmental progeroid phenotypes in humans and mice with genetic def
85 ough Sprtn hypomorphic mice recapitulate key progeroid phenotypes of RJALS, whether this model expres
86 vels and possibly link mechanisms leading to progeroid phenotypes to those of cell immortalization.
87  including cancer predisposition and various progeroid phenotypes, such as short lifespan, dwarfism,
88 ce results in changes in animal size but not progeroid phenotypes.
89 r syndrome (WS) is the canonical adult human progeroid ('premature aging') syndrome.
90                     Our results identified a progeroid-specific RT signature that is common to cells
91  we use a mouse model of the human XPF-ERCC1 progeroid syndrome (XFE) caused by loss of DNA repair.
92       Ercc1(-/Delta) mice model a rare human progeroid syndrome caused by inherited defects in DNA re
93                       Werner's syndrome is a progeroid syndrome caused by mutations at the WRN helica
94 ome (WS) is an autosomal recessive segmental progeroid syndrome caused by mutations in a novel member
95 ree patients are affected by a new segmental progeroid syndrome characterized by genomic instability
96              Werner syndrome (WS) is a human progeroid syndrome characterized by the early onset of a
97 tchinson-Gilford progeria syndrome (HGPS), a progeroid syndrome in children, is caused by mutations i
98 yndrome (WS) is a prototypic adult Mendelian progeroid syndrome in which signs of premature aging are
99                                          XFE progeroid syndrome is a disease of accelerated aging cau
100    Genetic studies of patients with neonatal progeroid syndrome led to the discovery of the novel fas
101 lar to that seen in cells from patients with progeroid syndrome resulting from a point mutation in BA
102          Ruijs-Aalfs syndrome is a segmental progeroid syndrome resulting from mutations in the SPRTN
103                               Similarly, XFE progeroid syndrome results from defects in the ERCC1-XPF
104 e WRN helicase gene cause Werner syndrome- a progeroid syndrome with an elevated risk of cancer and o
105 ford progeria syndrome (HGPS) is a segmental progeroid syndrome with multiple features suggestive of
106 search on Werner syndrome, a heritable adult progeroid syndrome with prominent dermatologic features,
107 sitive to oxygen and displays hallmarks of a progeroid syndrome, including early-onset mortality and
108   Loss of WRN causes the genomic instability progeroid syndrome, Werner syndrome.
109 of Ercc1 (-/) mice, a mouse model of a human progeroid syndrome, with the HSP90 inhibitor 17-DMAG ext
110 senchymal precursor cell (hMPC) model of the progeroid syndrome.
111 nked to chromatin alterations in an atypical progeroid syndrome.
112 s rare mutations in SPRTN that cause a novel progeroid syndrome.
113  a therapeutic approach for this devastating progeroid syndrome.
114 g in Werner and Bloom syndromes, but not XFE progeroid syndrome.
115  A, misshapen nuclei, and a lethal perinatal progeroid syndrome: restrictive dermopathy (RD).
116 deled after A-lamin (LMNA) mutations causing progeroid syndromes (PSs) in humans.
117 tant ramifications for DNA repair-deficient, progeroid syndromes and aging.
118  of L1 RNA in heterochromatin homeostasis in progeroid syndromes and identify a possible therapeutic
119  obvious cellular pathology in lamin-related progeroid syndromes and suggest a potential strategy for
120                                              Progeroid syndromes are rare genetic disorders that phen
121 mes might be involved in the pathogenesis of progeroid syndromes caused by defective RecQ helicases.
122 of prelamin A suggested that lamin A-related progeroid syndromes might be treated with impunity by re
123 er syndrome and a surprising number of other progeroid syndromes support the importance of the mainte
124 iety of congenital cancer susceptibility and progeroid syndromes that are caused by defects in genome
125 seases is illustrated by numerous congenital progeroid syndromes that are caused by mutations in geno
126 ibroblast cells from patients with different progeroid syndromes using specific antisense oligonucleo
127  upon multiple organs and tissues (segmental progeroid syndromes) and those that have their major imp
128 acts upon a single organ or tissue (unimodal progeroid syndromes).
129                                   Studies of progeroid syndromes, particularly HGPS, the most dramati
130 otent stem cells as a model for the onset of progeroid syndromes, we tracked the progression of RT ab
131      Single-gene mutations can produce human progeroid syndromes--phenotypes that mimic usual or "nor
132 rly event in both typical and atypical human progeroid syndromes.
133 Multiple genetic loci have been reported for progeroid syndromes.
134 protein p63 gene (TP63) as a gene marker for progeroid syndromes.
135 islocalization of XPA in laminopathy-related progeroid syndromes.
136 , cardiomyopathy, partial lipodystrophy, and progeroid syndromes.
137 NA(D300N) mutation is associated with DCM in progeroid syndromes.
138 , cardiomyopathy, partial lipodystrophy, and progeroid syndromes.
139 elope, cause misshapen nuclei, and result in progeroid syndromes.
140 eir rarity, diseases of premature aging, or "progeroid" syndromes, have provided important insights i
141 turnover of hundreds of abundant proteins in progeroid tissues.
142 ctivity of WRN, which is absent in the human progeroid Werner syndrome, is thought to counteract this
143                  Other DNA-repair-deficient, progeroid Xpg(-/-) (also known as Ercc5(-/-)) mice, a mo
144 span in physiologically aged mice as well as progeroid Zmpste24(-/-) mice that exhibit a premature ag

 
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