ライフサイエンスコーパス: cell aging

1 xual reproduction and cell senescence (i.e., cell aging).

2 resembling those acquired during human stem cell aging.

3 cell-cycle dynamics, and accelerated mother cell aging.

4 astic gene expression, cell cycle stages and cell aging.

5 e that asymmetric distribution drives mother cell aging.

6 rence for future epigenomic analysis of stem cell aging.

7 effects of somatic p16(INK4a) ablation on B-cell aging.

8 pt to anticipate how it might influence stem cell aging.

9 ng chromosome segregation, polar growth, and cell aging.

10 ng, suggesting DNA integrity influences stem cell aging.

11 ne chromosome 2 regulates hematopoietic stem cell aging.

12 damage reactions to proteins associated with cell aging.

13 we attempted to address how to reverse beta-cell aging.

14 gate what sirtuin 6 (SIRT6) does during beta-cell aging.

15 Netrin-1 as a critical regulator of BM niche cell aging.

16 ay important roles in both cell division and cell aging.

17 D4+ CD25+ CD127-Foxp3+) cells], markers of T cell aging [aged Th17 cells (CD3+ CD4+ IL17+ RORgammat+

18 play a critical role in tissue-specific stem cell aging and an increase in tissue fibrosis with age.

19 s of its biochemical and biological roles in cell aging and carcinogenesis.

20 hs), indicating substantial heterogeneity in cell aging and death.

21 of lipid oxidation is often associated with cell aging and death.

22 What molecular processes drive cell aging and death?

23 ccumulation of waste material contributes to cell aging and disease, dysregulation of lysosomal pH ma

24 a molecular portrait of progressive mammary cell aging and elucidate the transcriptional regulatory

25 elomere attrition is closely associated with cell aging and exposure to reactive oxygen species (ROS)

26 that the decline in lamin B1 underlies stem cell aging and impacts the homeostasis of adult neurogen

27 in gene silencing, chromosome stability, and cell aging and imply that lysine acetylation is a common

28 esign and test interventions that delay stem cell aging and improve both health and lifespan.

29 evisiae Sir2 protein known to be involved in cell aging and in the response to DNA damage, binds and

30 se evidences suggest that premature CD4(+) T-cell aging and lymphopenia induced spontaneous periphera

31 n (ETI), yeast cells have accelerated mother cell aging and mildly perturbed cell cycles.

32 ave recently been implicated in cancer, stem cell aging and pluripotency.

33 hypothesis is presented in which endothelial cell aging and survival are linked to molecular mechanis

34 egulated and can be targeted to reverse stem cell aging and tissue degeneration, giving hope for targ

35 Our findings link premature T cell aging and tissue-invasiveness to telomere deprotect

36 ck may have applications in the treatment of cell aging and tumorigenesis, although little is present

37 n of circadian clock proteins underlies stem cell aging and whether they are targetable for the allev

38 al role in inducing telomere loss, premature cell aging, and CD4 T-cell apoptosis or depletion via dy

39 in triggering telomere erosion, premature T-cell aging, and CD4 T-cell apoptosis or depletion via dy

40 d herein could be linked to nutrient stress, cell aging, and subsequent production of substances that

41 tanding the relationship between normal stem cells, aging, and cancer.

42 One hallmark sets naive T cell aging apart from most other tissues except stem cel

43 Molecular mechanisms underlying T-cell aging are beginning to be understood.

44 tered T cell function and accelerated immune cell aging as suggested by excessive telomere loss.

45 ine in stem cell function and rendering stem cell aging as the possible link between cellular aging a

46 ls, the role of the stem cell niche for stem cell aging as well as novel and encouraging experimental

47 rowth on soft agar, suggestive of inevitable cell aging attributable to expansion and possible transf

48 is not clear if the different onset of stem cell aging between individuals can be predicted or preve

49 berg et al. show that lymphoma accelerates T cell aging by transcriptional and epigenetic reprogrammi

50 usion, our data advance the concept of "stem cell aging" by establishing the critical role of lysosom

51 T cell aging contributes to the lower vaccine efficacy in

52 ome settings, the programs associated with T cell aging culminates in a maladaptive response that dir

53 evelopment of the most severe naive CD4(+) T cell-aging defects.

54 MGA2, to development, height, and mouse stem cell aging during late fetal development and young adult

55 circadian machinery directly regulates stem cell aging, especially in primates, remains poorly under

56 Finally, we ask whether stem cell aging establishes an epigenetic 'memory' that is in

57 w that long-term CR delays the onset of beta cell aging hallmarks and promotes cell longevity by redu

58 s model in two separate contexts of CD8(+) T cell aging: HIV infection and CAR T cell expansion in vi

59 To better understand T cell aging, improved measurements of age-related cellula

60 in chromosome stability, gene silencing and cell aging in eukaryotes and archaea.

61 we investigated phenotypic and functional T-cell aging in the rhesus macaques (RMs), currently the d

62 nd functional changes that occur during beta cell aging, including the transcriptional deregulation t

63 posed that supports the hypothesis that stem cell aging is at least partially due to an accumulation

64 sruptions of proteostasis contribute to stem cell aging is largely unexplored.

65 ion to demonstrating that hematopoietic stem cell aging is regulated by a distinct genetic element, e

66 lifespan cultured and uncultured epithelial cells, aging is associated with a reduction of myoepithe

67 In differentiated cells, aging is associated with hypermethylation of DNA

68 T cell aging manifests itself both at the cellular (cell-a

69 ive stress, lipid scrambling, and artificial cell aging modulate the cell response to the toxin.

70 n patients with rheumatoid arthritis (RA), T cell aging occurs prematurely, but the mechanisms involv

71 We suggest that some of the T-cell aging phenomenology in RMs can be ascribed to accen

72 Abca1/Abcg1-deficiency induces a premature T cell aging phenotype in middle-aged (12-13 months) Ldlr(

73 rategies to intervene in aspects of the stem cell aging process may have significant clinical relevan

74 In primary vascular smooth muscle cells, aging reduced proliferation, whereas conditioned

75 Molecular mechanisms of organismal and cell aging remain incompletely understood.

76 us-independent homeostatic disturbances in T cell aging remain unresolved.

77 A) is a biomarker of vascular smooth muscle cell aging that accelerates calcification however the me

78 Telomere length is a marker of cell aging that appears to be one mediator of this relat

79 w era of research on the epigenetics of stem cell aging that may represent therapeutic potential.

80 istic insights into HCV-mediated premature T-cell aging through miR-181a-regulated DUSP6 signaling an

81 ant neural subtypes, often with stressors or cell "aging", to enhance disease-specific phenotypes.

82 proteins, which are hypothesized to control cell aging via telomeric DNA interactions.

83 The acceleration of ETI mother cell aging was not explained by increased reactive oxyge

84 A new model for hematopoietic stem cell aging was proposed that supports the hypothesis tha

85 udy genetic regulation of hematopoietic stem cell aging, we have demonstrated definitively that a loc

86 pulations), noise, and density affect muscle cell aging, we introduce the mechanism of stochastic sur

87 tigate the role of PS exposure in normal red cell aging, we used N-hydroxysuccinimide-biotin to tag r

88 system, how long-term exercise affects stem cell aging, which is typified by reduced proliferative a

89 ectrode components and shortens the time for cell aging while improving the overall redox homogeneity

90 the association of epigenetic age and immune cell aging with sleep in the Women's Health Initiative s