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1 cular dystrophy, dilated cardiomyopathy, and Hutchinson-Gilford progeria syndrome.
2 letion including its processing site, causes Hutchinson-Gilford progeria syndrome.
3 MNA gene causes the premature aging disorder Hutchinson-Gilford Progeria Syndrome.
4 tling is altered in cells from patients with Hutchinson-Gilford progeria syndrome.
5 fflict the cardiovascular system and include Hutchinson-Gilford progeria syndrome.
6 celerated aging diseases Werner syndrome and Hutchinson-Gilford progeria syndrome.
7 kinson disease and a LMNA mutation linked to Hutchinson-Gilford progeria syndrome.
8 thies, including the premature aging disease Hutchinson-Gilford progeria syndrome.
9 sess changes in survival with treatments for Hutchinson-Gilford progeria syndrome.
10 ugs is now being tested for the treatment of Hutchinson-Gilford progeria syndrome.
11 luding Emery-Dreifuss muscular dystrophy and Hutchinson-Gilford progeria syndrome.
12 min A (LA) cause the premature aging disease Hutchinson-Gilford Progeria Syndrome.
13 ade in the most dramatic of these disorders, Hutchinson-Gilford progeria syndrome.
14 cular dystrophy, dilated cardiomyopathy, and Hutchinson-Gilford progeria syndrome.
15 xtends the lifespan in patients afflicted by Hutchinson-Gilford progeria syndrome, a devastating cond
16 rexpressed in fibroblasts from patients with Hutchinson-Gilford progeria syndrome, a form of accelera
17 e absence of primary neurological disease in Hutchinson-Gilford progeria syndrome, a genetic disease
18 teoporosis, which are phenotypes shared with Hutchinson-Gilford progeria syndrome, a human disease ca
19 nd myofibroblasts derived from patients with Hutchinson-Gilford progeria syndrome, a premature aging
20 herosclerosis is the main medical problem in Hutchinson-Gilford progeria syndrome, a rare premature a
21 the biology of premature aging uncovered in Hutchinson-Gilford progeria syndrome and other accelerat
22 with vascular smooth muscle cell loss (e.g., Hutchinson-Gilford progeria syndrome) and experimental s
23 hologies, including some forms of cancer and Hutchinson-Gilford Progeria Syndrome, and often include
24 vely good in comparison to that of classical Hutchinson-Gilford progeria syndrome, and we suggest tha
25 n wrinkling, and osteoporosis, patients with Hutchinson-Gilford progeria syndrome are affected by acc
26 the brain could explain why mouse models of Hutchinson-Gilford progeria syndrome are free of central
27 e used to study endothelial phenotype during Hutchinson-Gilford progeria syndrome-associated atherosc
28 cell line for the accelerated aging disease Hutchinson-Gilford progeria syndrome caused by mutant la
30 eus, and how this pathway is misregulated in Hutchinson-Gilford progeria syndrome, causing mTORC1 hyp
31 approach that reverts several alterations in Hutchinson-Gilford progeria syndrome cells and mice by i
34 se laminopathies such as the premature aging Hutchinson Gilford progeria syndrome (HGPS) and altered
35 hy diseases, restrictive dermopathy (RD) and Hutchinson Gilford progeria syndrome (HGPS), are charact
36 utosomal dominant premature ageing disorder--Hutchinson Gilford Progeria Syndrome (HGPS)-lead to redu
38 ure aging syndromes in humans, including the Hutchinson-Gilford Progeria Syndrome (HGPS) and Atypical
39 ascular calcification found in children with Hutchinson-Gilford progeria syndrome (HGPS) and in a mou
40 t cleavage cause the premature aging disease Hutchinson-Gilford progeria syndrome (HGPS) and related
42 characterized DNA RT program alterations in Hutchinson-Gilford progeria syndrome (HGPS) and Rothmund
43 Studies of the accelerated aging disorder Hutchinson-Gilford progeria syndrome (HGPS) can potentia
44 cytoplasmic Ran distribution is disrupted in Hutchinson-Gilford Progeria syndrome (HGPS) fibroblasts
77 tra-rare, pediatric premature aging disorder Hutchinson-Gilford progeria syndrome (HGPS) is caused by
87 ibroblasts from donors of different ages and Hutchinson-Gilford Progeria Syndrome (HGPS) patients.
91 tiple nuclear abnormalities in patients with Hutchinson-Gilford progeria syndrome (HGPS), a devastati
93 Ran are reduced in cells from patients with Hutchinson-Gilford progeria syndrome (HGPS), a disease c
94 colon, and acute myeloid leukemia as well as Hutchinson-Gilford progeria syndrome (HGPS), a genetic d
97 is a mutant form of lamin A responsible for Hutchinson-Gilford progeria syndrome (HGPS), a premature
100 both accelerated in patients suffering from Hutchinson-Gilford progeria syndrome (HGPS), a rare gene
101 ffort to develop experimental treatments for Hutchinson-Gilford progeria syndrome (HGPS), an endeavor
102 g protein 1 (SUN1), previously implicated in Hutchinson-Gilford progeria syndrome (HGPS), increase.
103 s redundancy suggests that diseases, such as Hutchinson-Gilford progeria syndrome (HGPS), that are ca
104 w, we highlight these recent developments in Hutchinson-Gilford progeria syndrome (HGPS), Werner synd
113 we introduce an inducible cellular model of Hutchinson-Gilford progeria syndrome in HeLa cells in wh
114 arly half of the world's known patients with Hutchinson-Gilford progeria syndrome, in a comprehensive
115 ssociated with pathological conditions as in Hutchinson-Gilford progeria syndrome, in which a mutatio
116 s, we determined that progerin expression in Hutchinson-Gilford progeria syndrome inhibits the nucleo
125 expression of a mutant Lamin A, progerin, in Hutchinson-Gilford Progeria Syndrome leads to alteration
126 rom two laminopathic mouse models, including Hutchinson-Gilford progeria syndrome (Lmna(L530P/L530P))
127 s that LMNA, a gene targeted for mutation in Hutchinson Gilford Progeria Syndrome, may control the on
133 y explains why "prelamin A diseases" such as Hutchinson-Gilford progeria syndrome spare the central n
134 responsible for the premature aging disease Hutchinson-Gilford progeria syndrome (termed progerin) a
135 rogerin (a toxic form of prelamin A found in Hutchinson-Gilford progeria syndrome), the levels of pro
139 responsible for the premature aging disorder Hutchinson-Gilford progeria syndrome, with its partners