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 cell-cycle dynamics, and accelerated mother cell aging.

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

4 e that asymmetric distribution drives mother cell aging.

5 rence for future epigenomic analysis of stem cell aging.

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

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

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

9 ng, suggesting DNA integrity influences stem cell aging.

10 ne chromosome 2 regulates hematopoietic stem cell aging.

11 damage reactions to proteins associated with cell aging.

12 resembling those acquired during human stem cell aging.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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